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Minipress (Prazosin)
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Minipress

Minipress is an effective strong preparation which is taken in treatment of hypertension diseases. Minipress is also helpful in treatment of male prostate enlargement symptoms, congestive heart failure, Raynaud's disease. Minipress acts as anti-hypertension remedy.

Other names for this medication:

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Lisinopril, Amlodipine, Norvasc, Benicar, Metoprolol, Hydrochlorothiazide, Avapro, Losartan

 

Also known as:  Prazosin.

Description

Minipress is created by pharmacy specialists to combat hypertension disease. Target of Minipress is to control level of blood pressure.

Minipress acts as anti-hypertension remedy. Minipress operates by reducing blood pressure.

Minipress is also known as Prazosin, Prazopress, Vasoflex, Hypovase.

Minipress is alpha blocker.

Generic name of Minipress is Prazosin (oral).

Brand name of Minipress is Minipress.

Dosage

You should take it by mouth with water.

It is better to take Minipress 2-3 times a day at the same time with meals or milk.

It is better to start the first Minipress dose when are going to bed.

If you want to achieve most effective results do not stop taking Minipress suddenly.

Overdose

If you overdose Minipress and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Minipress overdosage: feeling lightheaded, rash, weakness, troublesome breathing, pruritus, swelling.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Minipress are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Minipress if you are allergic to Minipress components.

Be careful with Minipress if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Minipress if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Minipress if you have allergies to medicines, foods, or other substances.

Be careful with Minipress if you have liver or kidney disease, heart failure, low blood pressure, narcolepsy, prostate cancer.

Be careful with Minipress if you take muscle relaxants as carisoprodol; anti-anxiety drugs as diazepam; anti-seizure drugs as carbamazepine; tranquilizers; sleep medicines as sedatives; antihistamines as diphenhydramine; verapamil; psychiatric medicines as tricyclic antidepressants (amitriptyline), phenothiazines (chlorpromazine); sexual function problems drugs as vardenafil, sildenafil, tadalafil; narcotic pain relievers as codeine; beta blockers as metoprolol, propranolol, atenolol.

Avoid machine driving.

Use Minipress with great care in case you want to undergo an operation (dental or any other).

Avoid alcohol.

Minipress can be not safety for elderly people.

Try to be careful with sunbeams. Minipress makes skin sensitive to sunlight. Protect skin from the sun.

Do not stop taking Minipress suddenly.

minipress medication information

To investigate the analgesic effect, rats were intraperitoneally administered with normal saline or various doses of ROE before or after a plantar incision. To evaluate the involved mechanism, rats were intraperitoneally administered yohimbine, dexmedetomidine, prazosin, naloxone, atropine, or mecamylamine after a plantar incision; ROE was then administered intraperitoneally. The mechanical withdrawal threshold (MWT) was tested with von Frey filaments at various time points. To determine the inflammatory response, serum levels of interleukin (IL)-1β or IL-6 were measured.

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A controlled-release gastrointestinal therapeutic system (GITS) formulation of doxazosin mesylate, a long-acting selective alpha1-adrenoceptor antagonist, was developed to enhance the pharmacokinetic profile and simplify the titration schedule by precisely controlling drug delivery rate, permitting an initial dose of 4 mg once daily, compared with standard doxazosin, which is initiated at 1 mg day-1 and titrated to a higher therapeutically effective dose. The aim of the present work was to evaluate the pharmacokinetics and bioavailability of doxazosin GITS with respect to the effect of food, age and gender, and multiple dosing. In addition, in vitro performance was assessed in conditions simulating the gastrointestinal environment.

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The properties and modulation by norepinephrine (NE) of voltage-dependent calcium currents were studied in bulbospinal neurons (n = 116) of the rostral ventrolateral medulla (RVLM) using whole cell patch-clamp techniques in neonatal rat brain stem slices. RVLM bulbospinal neurons were identified visually by their location in slices and by the presence of flourescein isothiocyanate-tagged microbeads, which were injected into the spinal cord before the experiment; RVLM neurons were filled with Lucifer yellow during recordings, and the slice was processed for detection of tyrosine hydroxylase immunoreactivity (TH-IR). Thirty-four of 42 recovered cells (81%) were positive for TH-IR, indicating that most recorded cells were C1 neurons. Bulbospinal RVLM neurons expressed a prominent high-voltage-activated (HVA) calcium current, which began to activate at -30 to -40 mV (from a holding potential of -60 or -70 mV), and peaked at approximately 0 mV (0.8 +/- 0.1 nA;mean +/- SE). HVA current comprised predominantly omega-conotoxin GVIA-sensitive, N-type and omega-agatoxin IVA-sensitive, P/Q-type components, with smaller dihydropyridine-sensitive, L-type, and residual current components. Most RVLM bulbospinal neurons (n = 44/52, including 12/14 histologically identified C1 cells) also expressed low-voltage-activated (LVA) calcium current. LVA current began to activate at approximately -60 mV (from a holding potential of -100 mV) and was nearly completely inactivated at -50 mV with a half-inactivation potential of -70 +/- 2 mV. The amplitude of LVA current at -50 mV was 78 +/- 24 pA with Ba2+ and 156 +/- 38 pA with Ca2+ as a charge carrier. NE inhibited HVA current in most bulbospinal RVLM neurons (n = 70/77) with an EC50 of 1.2 muM; NE had no effect on LVA current. Calcium current inhibition by NE was mediated by alpha2-adrenergic receptors (alpha2-ARs) as the effect was mimicked by the selective alpha2-AR agonist, UK-14,304, and blocked by idazoxan, an alpha2-AR antagonist, but unaffected by prazosin and propranolol (alpha1- and beta-AR antagonists, respectively). Most of the NE-sensitive calcium current was N- and P/Q-type. NE-induced inhibition of calcium current evoked by action potential waveforms (APWs) was significantly larger than that evoked by depolarizing steps (34 +/- 2.5 vs. 23 +/- 2.7%; P < 0.05). Although inhibition of calcium current was voltage dependent and partially relieved by strong depolarizations, when calcium currents were evoked with a 10-Hz train of APWs as a voltage command, the inhibitory effect of NE was maintained throughout the train. In conclusion, bulbospinal RVLM neurons, including C1 cells, express multiple types of calcium currents. Inhibition of HVA calcium current by NE may modulate input-output relationships and release of transmitters from C1 cells.

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The aortic pulse pressure (PP), which consists mainly of the incident wave and the reflected wave, has emerged as an important property of systemic blood vessels underlying the pathophysiology of cardiovascular disease. To determine the role of sympathetic nerve activity on the aortic PP response during dynamic exercise, we evaluated aortic hemodynamics during the right-leg knee-extension (40 and 60 % of maximal voluntary contraction) in six young adults with and without the systemic α1-adrenergic receptor blockade using prazosin (1 mg/20 kg body weight). The use of prazosin attenuated the exercise-induced increase in aortic PP (P < 0.05) but not in radial arterial PP. The amplitude of the reflected waves (via augmentation index) significantly decreased with the exercise and decreased more with the use of prazosin. These results suggest that during dynamic exercise the α1-adrenergic-mediated vasoconstrictor tone of the peripheral resistance vessels is manifestly involved in the magnitude of the reflected wave and the modulation of the aortic PP responses.

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Pheochromocytoma is associated with intense physiologic effects of alpha- and beta-adrenergic stimulation from catecholamine secretion. Perioperative management for these patients includes alpha-adrenergic receptor blockade, intravascular volume replacement, and, if necessary, beta-adrenergic receptor blockade. Significant perioperative changes in preload and afterload, fluid status, heart rate and rhythm, and inotropy can occur and may be contrary to anesthetic management goals for patients with certain conditions of congenital heart disease. We report the perioperative management with doxazosin of a patient with single ventricle physiology and cavo-pulmonary and aorto-pulmonary lung perfusion who presented for resection of a pheochromocytoma.

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Troglitazone is a thiazolidinedione used for the treatment of NIDDM and potentially for other insulin-resistant disease states. Troglitazone has recently been shown to increase cardiac output and stroke volume in human subjects. These actions are thought to be mediated by the reduction of peripheral resistance, but a potential direct effect on cardiac function has not been studied. Therefore, we investigated the direct cardiac hemodynamic effects of troglitazone in isolated perfused rat hearts. Five groups of hearts were studied. Hearts were tested under isovolumetric contraction with a constant coronary flow, and troglitazone (0.2, 0.5, and 1.0 micromol) was administered by bolus injection. Peak isovolumetric left ventricular pressure (LVPmax), peak rate of rise of LVP (dP/dt(max)), and peak rate of fall of LVP (dP/dt(min)) were significantly increased 1 min after troglitazone administration in a dose-dependent manner, while the heart rate (HR) and coronary perfusion pressure (CPP) were significantly decreased (P < 0.05). HR was then fixed by pacing and/or CPP was fixed with nitroprusside to eliminate any effect of the two variables on the action of troglitazone. With constant HR and/or constant CPP, the effect of troglitazone on LVPmax, dP/dt(max), and dP/dt(min) was still unchanged. In addition, the positive inotropic, positive lusitropic, and negative chronotropic actions of troglitazone were not influenced even when hearts were pretreated with prazosin, propranolol, or nifedipine. In conclusion, troglitazone has direct positive inotropic, positive lusitropic, negative chronotropic, and coronary artery dilating effects. The inotropic and chronotropic actions of troglitazone are not mediated via adrenergic receptors or calcium channels. These findings have important clinical implications for diabetic patients with congestive heart failure.

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Simple and sensitive spectrophotometric methods are described for the assay of three piperazine derivatives; ketoconazole, piribedil and prazosin hydrochloride based on charge-transfer and ion-pair complexation reactions. The first method is based on the reaction of the basic drug with 2,3-dichloro-5,6-dicyano-p-benzoquinone (DDQ) in acetonitrile. The orange-red colour formed due to the formation of charge-transfer complex showed maximum absorbance at 460 nm. The second method is based upon the interaction of the basic drug in dry chloroform with bromophenol blue (BPB) in the same solvent to produce a stable yellow ion-pair complex which absorbs at 410 nm. Beer's law was obeyed for both methods and the relative standard deviations were found to be less than 1%. The two methods can be applied to the analysis of tablets, with no evidence of interference from excipients. A more detailed investigation of the complex was made with respect to its composition, association constant and free energy change.

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The effects of l-amphetamine on the spontaneous firing of central neurons of African snails (Achatina fulica Ferussac) were studied electrophysiologically. The effects of dopamine, noradrenaline, d-amphetamine, and methamphetamine on the central neurons also were tested. The l- and d-amphetamines (0.3 mM) elicited bursting firing of action potentials in the RP4 neuron of the snail, whereas dopamine (0.3 mM), noradrenaline (NE, 0.3 mM), and methamphetamine (2 mM) did not. The bursting firing of action potentials elicited by l-amphetamine was decreased if potassium-free solution, sodium-free solution, or solution containing oubain (0.1 mM), a sodium pump inhibitor, was perfused. The results suggested that l-amphetamine did, and methamphetamine did not, elicit a sodium-dependent bursting firing of action potentials of the neuron.

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This study aimed at assessing whether chronic stress induces vascular alterations, and whether these modulations are nitric oxide (NO) and Ca(2+) dependent.

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Four pharmacons were tested on an acute portal pressure lowering effect in an experimental animal model with 25 normal and 25 rats with Thioacetamide-toxic liver cirrhosis. Invasive measurements of arterial and portal pressure were made under Hexobarbital-Sodium anaesthesia during 30 minutes after pharmacon application. The portal pressure of cirrhotic rats was under basic conditions 9.5 +/- 1.5 mm Hg and significant higher as in normal animals (5.3 +/- 0.9 mm Hg, p less than 0.01). After 10 mg/kg body mass Propranolol the portal pressure decreased in both animal groups small but not significantly over the whole measurement time. 1 mg/kg Verapamil lowered arterial middle pressure significantly, but increased portal pressure at all 15-20% in both animal groups. Application of 0.1 mg/kg Prazosin decreased the arterial middle pressure at all 5-15% and the portal pressure at all 20-30% in both study groups (both significantly). For Canrenoat-Potassium (20 mg/kg) no clear effect could by evaluated on portal pressure. The model of Thioacetamide-toxic cirrhosis of the rat offers conditions like cirrhosis in human medicine in order to study the effects of portal pressure lowering pharmacons. Propranolol and Prazosin decrease portal pressure and should by further investigated.

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These results suggest that presynaptic or central alpha2-adrenoceptor function, or both, is specifically impaired after 9 weeks of a high-fat diet. These modifications may account for the development of arterial hypertension in this model.

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To evaluate the effect of electroacupuncture (EA) on symptomatic benign prostatic hyperplasia (BPH).

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Antagonism of alpha 1-adrenoceptor-mediated vascular contraction by urapidil was examined in helical strips of femoral and mesenteric arteries isolated from 13-week-old Aoki spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto (WKY) rats, since this agent has antihypertensive effect through antagonizing peripheral alpha-adrenoceptors. Schild plot analyses clearly demonstrated the existence of only alpha 1-adrenoceptors in these arteries from both strains. Therefore, it is possible to demonstrate alpha 1-adrenoceptor blocking effects of nonselective alpha-adrenoceptor antagonists as well as selective alpha 1-adrenoceptor antagonists. Urapidil antagonized the alpha 1-adrenoceptor-mediated vascular contraction in a competitive fashion. The pA2 value for urapidil against alpha 1-adrenoceptors was not significantly different between SHR and WKY rats. The addition of 10(-5) M norepinephrine (NE) produced a sustained contraction in a SHR femoral artery, whereas in a WKY rat femoral artery this agonist produced a transient contraction followed by a sustained relaxation. Urapidil elicited a dose-dependent relaxation with a IC50 value of 6.50 in the SHR femoral artery precontracted with NE. In the presence of 3 x 10(-7) M timolol, a beta-adrenoceptor antagonist, femoral arteries from both strains exhibited similar magnitude of contraction in response to the stimulation with 10(-5) M NE. Under these conditions, urapidil elicited a similar extent of relaxation between SHR and WKY rats. On the other hand, the addition of 10(-5) M NE produced a sustained contraction in mesenteric arteries from both SHR and WKY rats. The contraction expressed as a ratio to the maximum developed by KCl depolarization was significantly greater in SHR than in WKY rats. In these arteries, the relaxing effect of urapidil was more evident in SHR than in WKY rats. Contractile responses to NE and relaxing effects of urapidil were not affected by timolol. These results suggest that urapidil effectively antagonized enhanced alpha 1-adrenoceptor responses seen in SHR arteries.

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The affinity of 5-methyl-urapidil for alpha 1-adrenoceptors was determined from the inhibition of [3H]prazosin binding on membrane of different rat tissues. In hippocampus, vas deferens and heart 5-methyl-urapidil displaced [3H]prazosin in a biphasic manner with mean pKI values between 9.1 and 9.4 for the high-affinity site and 7.2 to 7.8 for the low-affinity site. Only the low affinity site was found in spleen and liver. At present, 5-methyl-urapidil is the antagonist which most clearly discriminates between alpha 1-adrenoceptor subtypes.

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Evoked noradrenaline release was monitored every 1 s in vivo from the hypothalamic paraventricular nucleus by differential pulse amperometry at +105 mV combined with carbon fiber electrodes. Noradrenaline release was evoked by electrical stimulations of the ventrolateral medulla for 20s every 10 min at a physiological frequency (3-20 Hz) (see accompanying paper). The evoked noradrenaline release was dose-dependently attenuated by clonidine (10-100 micrograms/kg, i.v.) and strongly enhanced by alpha-2 antagonists: yohimbine (2 mg/kg), piperoxane (2 mg/kg) and idazoxan (0.05-1 mg/kg). Moreover, the effect of clonidine (50 micrograms/kg) was prevented by yohimbine (5 mg/kg) or idazoxan (1 mg/kg). Haloperidol (50 micrograms/kg) or propranolol (10 mg/kg) did not affect evoked noradrenaline release while prazosin (0.05-1 mg/kg) induced a moderate increase. However, prazosin did not prevent the effect of clonidine (50 micrograms/kg). Reserpine (5 mg/kg) pretreatment for 1 h induced a pronounced decrease in the evoked noradrenaline release and abolished the effect of yohimbine (2 mg/kg). Pretreatment by desipramine 30 min before injection abolished the effect of clonidine (50 micrograms/kg) but not of yohimbine (2 mg/kg). The amplitude of the yohimbine (2 mg/kg) effect depended on the frequency of the stimulation: it was maximal between 3 and 7 Hz and gradually declined from 10 to 20 Hz. These results show that noradrenaline release is presynaptically controlled by an alpha-2 adrenoreceptor and suggest that, in physiological conditions, endogenous extracellular noradrenaline inhibits its own phasic release. In conclusion, noradrenergic terminals act as a high pass filter which converts impulse flow into noradrenaline release and the features of this filter are modulated by extracellular noradrenaline via an alpha-2 adrenoreceptor.

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The noradrenalin-evoked production of [3H]inositol phosphates in mouse striatal astrocytes in primary culture appeared to be the result of the combined stimulation of alpha 1- and alpha 2-adrenergic receptors. Indeed, the noradrenalin (100 microM) response was only partially reproduced by a maximally effective concentration of methoxamine (100 microM), a selective agonist of alpha 1-adrenergic receptors. In addition, the noradrenalin (100 microM)-induced production of [3H]inositol phosphates, which was completely suppressed by the alpha 1-adrenergic antagonist prazosin (1 microM), was also partially inhibited by yohimbine, a selective antagonist of alpha 2-adrenoceptors (maximum inhibition = -57 +/- 11%, measured in the presence of 10 microM yohimbine; six experiments). Finally, UK14.304, a selective alpha 2-adrenergic agonist that was ineffective alone, enhanced the methoxamine-evoked production of [3H] inositol phosphates (EC50 = 86 +/- 21 nM; three experiments). These results suggest that the stimulation of alpha 1-adrenergic receptors is required for the alpha 2-adrenergic receptor-mediated enhancement of phospholipase C activity. The increased production of [3H]inositol phosphates resulting from the stimulation of alpha 2-adrenergic receptors involved pertussis toxin-sensitive G proteins (Gi/o) and depended on extracellular calcium. As shown using the fluorescent dye indo-1, noradrenalin (100 microM) induced a long-lasting increase in cytosolic calcium in striatal astrocytes. Moreover, noradrenalin (100 microM) stimulated [3H]arachidonic acid release from these cells. These two latter responses may result from synergistic effects due to the combined stimulation of alpha 1- and alpha 2-adrenergic receptors, because they were inhibited by either prazosin (1 microM) or yohimbine (10 microM). Finally, the noradrenalin-evoked production of [3H]inositol phosphates seems to result partly from an inhibition by arachidonic acid of glutamate uptake into astrocytes, leading to the stimulation of glutamate metabotropic receptors coupled to phospholipase C. Indeed, the alpha 2-adrenergic component of the noradrenalin response was suppressed by either enzymatic removal of external glutamate or addition of 2-amino-3-phosphonopropionic acid (1 mM), an antagonist of glutamate metabotropic receptors that blocked the glutamate-evoked production of [3H]inositol phosphates in striatal astrocytes, and was reproduced by the direct application of either glutamate or an inhibitor of glutamate uptake, beta-methyl-DL-aspartic acid.

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In vitro long-term facilitation (ivLTF) is a novel form of activity-independent postsynaptic enhancement of AMPA receptor function in hypoglossal (XII) motoneurons that can be induced by intermittent activation of 5-HT2 receptors. In vivo respiratory long-term facilitation (LTF) is characterized by a persistent 5-HT2 receptor-dependent increase in respiratory motor output or ventilation after episodic exposures to hypoxia in adult rats. Here, we demonstrate that ivLTF can also be induced by episodic but not continuous stimulation of alpha1-adrenergic receptors that requires protein kinase C (PKC), but not PKA (protein kinase A), activation. Additionally, we show that in vivo respiratory LTF is also alpha1-adrenergic receptor dependent. We suggest that, in vivo, concurrent episodic activation of 5-HT2 and alpha1-adrenergic receptors is necessary to produce long-lasting changes in the excitability of respiratory motoneurons, possibly involving PKC activation via the G alpha(q)-PLC (phospholipase C) signaling pathway common to both receptor subtypes. Such plasticity of XII motor output may increase upper airway muscle (innervated by XII nerve) tone and improve the likelihood that airway patency will be maintained. Elucidating the mechanism underlying LTF can be of clinical importance to the patients suffering from sleep-disordered breathing.

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We identified 69 men with symptomatic benign prostatic hyperplasia (BPH) who had been receiving 5 mg/day (n = 33) of finasteride or 2 to 5 mg/day (n = 14) of terazosin or no therapy ("watchful waiting") (n = 22). The three groups were compared with respect to pretreatment total serum PSA levels and post-treatment total, free, and percent free serum PSA levels.

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The activation of p70(S6) kinase and JNK2 may be implicated in the development of catecholamine-induced cardiac hypertrophy in vivo.

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The role of spinal mechanisms in subcutaneous (s.c.) nicotine-induced antinociception was examined in male Sprague-Dawley rats using the hot-plate and tail-flick tests. Nicotine (0.125, 0.25, 0.375 or 0.5 mg/kg s.c.) produced a dose-related inhibition of nociception in both tests. Although increasing negative geotaxis response times slightly, no significant alteration of other motor reflexes was observed with 0.375 mg/kg of s.c. nicotine. Microinjection of 7 nmol of the high-affinity choline uptake inhibitor hemicholinium-3 into the rostral ventral medulla completely inhibited the antinociception produced by 0.375 mg/kg of s.c. nicotine. Intrathecal (i.t.) injection of 61 nmol of nicotine (in 10 microliter buffer) produced no changes in hot-plate or tail-flick test response latencies. Nicotine-induced antinociception was blocked by a variety of i.t. antagonists injected 12 min before s.c. injection of 0.375 mg/kg of nicotine. In both tests, i.t. pretreatment with 0.1 mumol (in 10 microliter buffer) of scopolamine, methysergide, yohimbine, idazoxan, mecamylamine or 0.2 mumol of atropine attenuated nicotine-induced increases in test response latencies. Pretreatment with 0.1 mumol of atropine attenuated nicotine-induced increases in tail-flick test, but not in the hot-plate test. Pretreatment with 0.1 mumol of i.t. prazosin or naloxone produced no changes in nicotine-induced increases in test response latencies in either test. These data suggest that the antinociception produced by s.c. nicotine is mediated via a number of sites in the spinal cord, including alpha-2 adrenergic, serotonergic and muscarinic cholinergic.(ABSTRACT TRUNCATED AT 250 WORDS)

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alpha 1-Adrenoceptors (ARs) were divided into alpha 1H and alpha 1L subtypes by their different affinities for bunazosin or prazosin. alpha 1H-ARs were further subdivided into alpha 1A, alpha 1B, and alpha 1C subtypes. Therefore, this study was undertaken to determine which alpha 1-AR subtypes were involved in the activation of femoral artery preparations by alpha 1-AR agonists in spontaneously hypertensive rats (SHR). For comparison, aortic strips were also incorporated in the present study. In the presence of propranolol, deoxycorticosterone, and desipramine, norepinephrine (NE) contracted the vascular strips in a dose-dependent manner. Negative log EC50 values and maximum responses of NE-induced contraction of the SHR femoral artery were unchanged and increased, respectively, compared with those of Sprague-Dawley and Wistar-Kyoto rats (WKY). Contractile responses of the SHR aortae to NE were similar to those of the normotensive tissues. Schild plot data for alpha 1-AR antagonists indicated that alpha 1-AR subtypes mediating contraction of the aorta were homogeneous and had high affinities for bunazosin (pA2 9.4, alpha 1H subtype) and WB 4101 (pA2 9.3) and a low affinity for 5-methylurapidil (pA2 7.7). In the femoral artery, because Schild plots for bunazosin had slopes of less than 1.0, there were alpha 1H and alpha 1L subtypes. Bunazosin, at 10(-9) M, which could mask the alpha 1H subtype, yielded a Schild plot for bunazosin with a slope not different from unity and decreased the pA2 value for bunazosin (pA2 9.4 vs. 8.5).(ABSTRACT TRUNCATED AT 250 WORDS)

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To assess the effects of doxazosin, a selective alpha 1 adrenoceptor inhibitor, on blood pressure and urinary flow in normotensive and hypertensive (sitting diastolic blood pressure more than 90 mm Hg) men with prostatic hyperplasia (BPH).

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The results support a role of the SNS in driving the chronic visceral and somatic hypersensitivity seen in CI rats. The findings further suggest that treatments that decrease sympathetic outflow or block activation of adrenergic receptors on sensory nerves could be beneficial in the treatment of generalized pain syndromes.

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Calcium antagonists blunt the constrictor effects of vasoconstrictor agents. Differences in the sensitivity of several vasoconstrictors to the constrictor effect of calcium antagonists were quantified in experiments on rats and rabbits. In rats, the dose-response curves for pressor effects to angiotensin II were shifted in parallel to the right after treatment with isradipine, but not with prazosin and dihydralazine, suggesting that the antivasoconstrictor effect of isradipine was of a specific type. Blood pressure increases elicited by angiotension II or norepinephrine (alone, or with propranolol or propranolol plus prazosin) were also measured in rabbits and, again, isradipine caused parallel shifts of the dose-response curves. Both agonists thus appear to stimulate calcium entry, at least in resistance vessels, and via the same pathway, the L-type calcium channel. However, the angiotension II pressor effects were more sensitive to isradipine than those of norepinephrine in the presence of propranolol, and even more so in the presence of propranolol plus prazosin. These results suggest subtle and as yet unexplained differences, possible related to the activity of the adenylate cyclase system, in the chain of events leading to activation of the L-channels in vivo.

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minipress overdose 2016-07-29

The aim of this study was to determine the contribution of alpha 2- and alpha 1-adrenoceptor agonist activity of the formamidine, amitraz, on peripheral circulation in the dog. Intra-arterial injections of amitraz (0.25-5.0 micrograms/kg) produced a dose-dependent increase in perfusion pressure in the autoperfused hind limbs of methoxyflurane-anaesthetized dogs. A constant blood flow to the hind limbs was maintained using a peristaltic pump. Intravenous phentolamine (0.5 mg/kg), prazosin (35 micrograms/kg) and yohimbine (10 micrograms/kg) in separate experiments antagonized the vasoconstrictor actions of amitraz and produced a parallel shift to the right of the amitraz dose-response curve. Cumulative doses of amitraz (0.5-15 micrograms/kg) given by intracisterna magna (i.c.m.) injections reduced mean arterial pressure and heart rate in a dose-dependent manner. Similar responses were produced by intravenous amitraz but at much higher doses. In separate experiments amitraz-induced hypotension (doses up to 25 micrograms/kg i.c.m.) was buy minipress prevented by pre-treatment with yohimbine (30 micrograms/kg i.c.m.) but not prazosin (20 micrograms/kg i.c.m.). Both antagonists partially inhibited the bradycardia produced by amitraz. It is concluded that amitraz stimulates alpha 1- and alpha 2-adrenoceptors to produce vascular constriction. The central hypotensive action of amitraz appears to be mediated by alpha 2-adrenoceptors; however, both receptor subtypes appear to be stimulated to produce bradycardia.

minipress dosage forms 2015-09-30

The objective of this study was to explore the involvement of monoamines in the antidepressant-like effect of AECSF in buy minipress mice.

minipress dosage 2017-09-24

Calcium ionophore A23187 or phenylephrine injected i.p. in doses of 0.05-0 .25 mg kg-1 and 0.1-1 mg kg-1, respectively, induced translocation of protein kinase C (PKC) from the cytosol to the membrane fraction of the rat frontal cortex and hippocampus. The action of A23187 was blocked in a dose-dependent manner by nifedipine and verapamil. The phenylephrine induced translocation of PKC was blocked by prazosin and in a dose-dependent manner by nifedipine and verapamil. In contrast, pre-treatment with a small, ineffective by itself, dose of A23187 (0.02 mg kg-1) potentiated the alpha1-adrenoceptor induced translocation of buy minipress PKC. Thus, it seems that the influx of calcium ions through an L-type calcium channel is probably necessary for a full alpha1-adrenoceptor mediated activation and translocation of PKC.

minipress 4 mg 2016-08-18

The antihypertensive efficacy and safety of doxazosin, a selective alpha 1-inhibitor, were assessed in 33 severely hypertensive patients. The study involved three phases: a 1-day baseline period, a 32-day period in which patients received doxazosin, 1 to 16 mg, once daily, and a 4-week maintenance period. All patients were considered therapy successes (sitting diastolic blood pressure either less than or equal to 90 mm Hg or greater than or equal to 10 mm Hg reduction) at a mean daily dose of 8.1 mg. Twenty-seven patients (82%) achieved good blood pressure control (sitting diastolic blood pressure less than or equal to 90 mm Hg) at a mean dose of 6.7 mg once daily. By the final treatment visit, mean systolic/diastolic blood pressures in the sitting and supine positions were significantly reduced by 40/29 and 37/28 mm Hg from a mean baseline of 180/121 and 181/121 mm Hg to final visit values of 140/91 and 144/92 mm Hg, respectively (p less than 0.05). Eleven patients experienced one or more side effects that were mild or moderate and disappeared or were tolerated with continued therapy. During the study no abnormal laboratory test findings were identified by the investigators. The investigators' global assessment of the efficacy and toleration of once-daily doxazosin therapy was excellent or good for 31 (94%) patients and fair for buy minipress the remaining two patients.

minipress nightmares dosage 2016-09-22

Moxonidine is an antihypertensive drug that lowers sympathetic vasomotor tone by stimulating either alpha2-adrenergic (alpha2-AR) or imidazoline I1 receptors within the rostral ventrolateral medulla (RVL). In this study, we investigated the effects of moxonidine (10 microM) on RVL neurons in brain stem slices of neonatal rats. We recorded mainly from retrogradely labeled RVL bulbospinal neurons (putative presympathetic neurons) except for some extracellular recordings. Prazosin was used to block alpha1-adrenoceptors. Moxonidine inhibited the extracellularly recorded discharges of all spontaneously active RVL neurons tested (bulbospinal and unidentified). This effect was reversed or blocked by the selective alpha2-AR antagonist SKF 86466 (10 microM). In contrast, the I1 imidazoline ligand AGN 192403 (10 microM) had no effect on the spontaneous activity. In whole cell recordings (holding potential -70 mV), moxonidine produced a small and variable outward current (mean 7 pA). This current was observed in both tyrosine hydroxylase-immunoreactive and other bulbospinal neurons and was blocked by SKF 86466. Excitatory postsynaptic currents (EPSCs) evoked by focal electrical stimulation were isolated by incubation buy minipress with gabazine and strychnine, and inhibitory postsynaptic currents (IPSCs) were isolated with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Moxonidine reduced the amplitude of the evoked EPSCs (EC(50) = 1 microM; 53% inhibition at 10 microM) but not their decay time constant (5.6 ms). The effect of moxonidine on EPSCs persisted in barium (300 microM) and was reduced approximately 80% by SKF 86466. Moxonidine also reduced the amplitude of evoked IPSCs by 63%. In conclusion, moxonidine inhibits putative RVL presympathetic neurons both presynaptically and postsynaptically. All observed effects in the present study are consistent with an alpha2-AR agonist activity of moxonidine.

minipress xl dosage 2016-02-14

To compare the efficacy of Dobutamine and Prazosin in the management of buy minipress cases with scorpion sting.

minipress drug 2017-03-06

In the central nervous system neurotransmitters, drugs or conditions that excite increase cyclic guanosine 3',5'-monophosphate ( buy minipress cGMP), an effect mediated by the neuromodulator nitric oxide, whereas those that sedate decrease cGMP. Volatile anesthetics were shown to decrease cerebellar cGMP, an effect that correlates with their anesthetic and anticonvulsant effect. Because alpha-2 adrenoceptor agonists have anesthetic properties, the role of the nitric oxide-cGMP pathway in the action of the alpha-2 adrenoceptor agonists clonidine and dexmedetomidine was investigated.

minipress xl tablets 2016-05-28

Classical antipsychotics exemplified by haloperidol (0.30), fluphenazine (0.070) and cis(Z)-flupentixol (0.088; ED50 values in mumol/kg are given in parentheses for all compounds) potently block the discriminative stimulus properties of D-amphetamine (1.0 mg/kg, IP) in rats. Newer antipsychotics have very different buy minipress profiles: clozapine (7.2) and olanzapine (5.9) induce dose-dependent inhibition, while risperidone (> 6.1) and remoxipride (> 47) show weak inhibitory effects and sertindole (> 23), seroquel (> 20), amperozide (> 2.9) and the putative antipsychotic MDL 100151 (> 13; racemate with MDL 100907 as the active enantiomer) are ineffective. Antagonists of alpha 1-adrenoceptors (prazosin; > 6.0), 5-HT2A/2C (ritanserin; > 2.6) and histamine H1 receptors (mepyramine; > 50) are ineffective. Sertindole (0.076), risperidone (0.23), clozapine (0.39), olanzapine (0.088), MDL 100151 (0.0082), fluphenazine (0.13) and ritanserin (0.12) are potent inhibitors of the discriminative stimulus induced by the 5-HT2A/2C agonist DOI (0.63 mg/kg, IP), while haloperidol (approximately 0.4), cis(Z)-flupentixol (approximately 0.04), amperozide (approximately 0.5) and prazosin (> 12) show partial inhibition and remoxipride (> 23) and mepyramine (> 25) are ineffective. The results indicate that inhibition of D-amphetamine discrimination does not correlate with antipsychotic activity of newer antipsychotics, as has previously been suggested in the literature. Furthermore, the inhibitory potencies against D-amphetamine-induced discrimination (present study) and hypermotility (previous study in the same strain of rats) do not correlate either for several of the newer antipsychotics (e.g. for sertindole, risperidone, seroquel and remoxipride). The discrepancies cannot solely be explained by additional pharmacological effects of these compounds, e.g. 5-HT2 receptor blockade. The D-amphetamine discrimination is documented to depend on increased limbic dopamine function which in humans is associated with increased euphoria. Based on these results, it is hypothesized that D-amphetamine discrimination rather than a model for antipsychotic activity may reflect dysphoric or anhedonic activity.

tab minipress dose 2016-12-06

Human subjects with impaired baroreflex function cannot buffer rises or falls in blood pressure (BP), thus allowing BP effects of endogenous or buy minipress environmental stimuli that previously escaped detection to emerge dramatically. Studies in these patients led us to discover that water ingestion induced a robust increase in BP and vascular resistance. Here, using a mouse model of baroreflex impairment, we show that the increase in blood pressure after water ingestion is mediated through sympathetic nervous system activation and that the osmosensitive transient receptor potential vanilloid 4 channel (Trpv4) is an essential component of the response. Although portal osmolality decreases after water ingestion in both wild-type and Trpv4(-/-) mice, only the wild-type animals show a pressor response. The same volume of physiological saline does not elicit an increase in BP, suggesting osmolality as the stimulus. The osmopressor response to water, and Trpv4 thus represent new factors now implicated in the physiology of BP regulation.

minipress drug class 2016-12-26

K+ and Na+ influx into frog erythrocytes incubated in standard saline was studied using 86Rb and 22Na as tracers. 10 microM isoproterenol (ISP) produced a significant increase in K+ influx for the first 15 min, which was sustained during the entire 60 min of cell incubation. Treatment of red cells with the phosphodiesterase (PDE) blockers theophylline (THEO, 1 and 5 mM) or 3-isobutyl-1-methylxanthine (IBMX, 0.5 mM) was also accompanied by an enhancement in K+ influx. A distinct additive effect on K+ influx into red cells was found when ISP and THEO or IBMX were added together. The increase in K+ transport induced by ISP plus IBMX was totally abolished by pretreatment of red cells with 0.1 mM ouabain. The ouabain-sensitive K+ influx in frog erythrocytes was buy minipress elevated in the presence of ISP plus IBMX to 2.05 +/- 0.45, as compared with the control level of 0.39 +/- 0.11 mmol/L cells/hr (P < 0.001). Similar effects of ISP and IBMX on K+ influx were observed after chloride was replaced by nitrate. A dose-related increase in K+ influx into frog erythrocytes was observed at ISP concentrations of 10(-8)-10(-6) M, with a half-maximal stimulatory concentration of approximately 0.02 microM. The effects of ISP (10(-8)-10(-5) M) on K+ transport were completely abolished with 10 microM of the beta-adrenergic blocker propranolol, but alpha-adrenergic antagonists (phentolamine, prazosin, and yohimbine) did not alter the ISP-induced increase in K+ influx. The drugs tested had no effect on 22Na influx in frog red cells, but ISP produced a small decline (13%) in intracellular Na+ concentration. Thus, our study indicates that catecholamines and PDE blockers enhance K+ (86Rb) transport in frog erythrocytes mediated by Na(+)-K+ pump activity. The frog erythrocyte membrane may serve as a convenient model to investigate the hormonal modulation of the Na(+)-K+.

minipress 2 mg 2016-04-27

The alpha-adrenergic antagonists phentolamine and prazosin were administered to male rats to explore their effects on cold-induced TRH release, measured by a chronic push-pull cannula stereotaxically implanted in the median eminence (ME). Phentolamine was given either i.p. (24 or 40 mg/kg), or locally (10(-5) M) in the ME, whereas prazosin was only applied locally (10(-5) M). Phentolamine significantly decreased the cold response buy minipress (5 +/- 1 pg/15 min vs 21 +/- 5 pg/15 min; P less than 0.02), whatever the administration mode. Moreover, the blocking effect of prazosin directly perfused into the ME (11 +/- 3 pg/15 min vs 26 +/- 9 pg/15 min; P less than 0.05), indicates the specific involvement of alpha 1-adrenergic receptors in the cold-induced TRH response, and points to the ME as a possible site of facilitatory adrenergic control.

minipress overdose death 2017-03-14

This study was intended to quantify the amounts of the alpha1-adrenoceptor subtype mRNAs in human renal artery and to demonstrate the distribution of receptor subtypes responsible for the contraction of the renal artery. RNase protection assay showed that the mean amount of alpha1a mRNA was much greater than that of alpha1b or alpha1d mRNAs in both the main and branch renal arteries. However, the abundance of alpha1a mRNA in human renal artery was much less than in our previous data in the prostate. In situ hybridization showed that all alpha1 subtype mRNAs were localized in the smooth muscle cells of the tunica media of the artery, and the distribution pattern of these three mRNAs in the main artery was the same as in the branch artery. However, the intensity of signals for alpha1d and alpha1b antisense RNAs probes was lower than that for the alpha1a antisense RNA probe. In the functional study, concentration-response curves to noradrenaline pretreated with KMD-3213, an alpha1A/L-adrenoceptor selective antagonist, seemed to be biphasic in nature. Chloroethyclonidine (CEC) failed to inactivate the noradrenaline-induced contraction, and prazosin showed relatively low affinity with a pA2 value of 8.8. These data suggest that the alpha1A/L-adrenoceptor mediates primarily those buy minipress responses to noradrenaline in this artery. The other alpha1-adrenoceptor subtypes could also mediate the secondary contractile response to noradrenaline in this artery.

minipress medication 2017-05-20

In the present study, we examined the effects of alpha(1)- and the alpha(2)-adrenoceptors blockade on the changes in the ventricular content of catecholamines in rats withdrawn from morphine. Rats were given morphine by s.c. implantation of morphine pellets for 5 days. On the seventh day, morphine withdrawal was induced by s.c. administration of naloxone (1 mg/kg), and rats were killed 30 min later. Pretreatment with yohimbine (alpha(2)-adrenoceptor) or prazosin (alpha(1)-adrenoceptor) 15 min prior to naloxone administration attenuated some of the behavioural signs of morphine withdrawal. In addition, biochemical analysis indicated that yohimbine completely abolished the withdrawal-induced increase in noradrenaline and dopamine turnover in the right ventricle. By contrast, prazosin did not block the hyperactivity of Cymbalta Generic Availability catecholaminergic neurons in the heart during withdrawal. These data suggest that the hyperactivity of catecholaminergic neurons in the heart during morphine withdrawal is dependent upon alpha(2)-adrenoceptor activation. In addition, the present results rule out the involvement of alpha(1)-adrenoceptors.

tab minipress dosage 2016-04-19

1. We previously found that adrenaline and noradrenaline exert essentially opposite effects on clearance from plasma of chylomicron-like emulsions injected intravenously in rats, suggesting mechanisms that may be implicated in the atherogenic effects of chronic stress and hypertension and conversely in the protective effect of regular exercise. 2. The mechanisms underlying the effects of adrenaline and noradrenaline have now been investigated. Chronic adrenergic blockade with either the alpha 1-receptor antagonist doxazosin or the beta-receptor antagonist propranolol slowed the clearance of labelled emulsion lipids from plasma of normal Wistar rats. The results with doxazosin were unexpected in view of its capacity to decrease plasma triglycerides in patients. 3. In spontaneously hypertensive rats (SHR) the clearance of triolein (TO) was very slow compared with normal Wistar rats. Emulsion TO clearance provides a measure of lipolysis by lipoprotein lipase, and a defect in clearance indicates either defective enzyme action or poor perfusion of capillary beds rich in enzyme. Defective enzyme activity in SHR was excluded, suggesting redistribution of blood flow away from skeletal muscle and adipose tissue. In SHR the TO clearance from injected chylomicron-like emulsions was improved by blockade with doxazosin compared with control untreated SHR. 4. The beta 2-adrenoreceptor agonist Fenoterol was infused intravenously during clearance of an injected lipid emulsion. Clearance of radiolabelled cholesteryl oleate (CO) was clearly slowed while there was a lesser reduction of TO clearance rate. Emulsion CO clearance provides a measure of the uptake of lipoprotein remnants by the liver, and a defect in clearance of CO indicates either defective ligand (apolipoprotein E)-receptor interaction or decreased perfusion of the splanchnic bed. Isoprenaline, a non-selective beta-adrenergic agonist, gave similar results. Both compounds reduced mean arterial pressure by about 20-40 mm Hg at the doses employed, indicating that the beta 1 (cardiac) effect of the isoprenaline was insufficient to offset its vasodilatatory effect on skeletal muscle arterioles (beta 2). 5. The Diflucan Maintenance Dose alpha-agonist phenylephrine, at a dose which moderately raised mean arterial pressure, slowed clearance of both TO and CO for the first 12 min after injection of emulsion but at later time points clearances caught up with the controls. 6. Administration of a mixture of isoprenaline and phenylephrine produced definite enhancement of both TO clearance and CO clearance. The effect of the mixture was opposite to the effects of of either agonist alone, demonstrating clearly that direct effects on lipoprotein lipase activity or receptor mediated processes were not involved.(ABSTRACT TRUNCATED AT 400 WORDS)

minipress cost 2016-04-30

The purpose of this study was to investigate the possibility that sympathetic exacerbation of neuropathic pain activity may be mediated in part by the development of abnormal peripheral adrenergic mechanisms at the site of peripheral nerve injury. We evaluated changes in mechanical stimulation withdrawal thresholds before and after the delivery of selected alpha-adrenergic agonists and antagonists to the immediate area of a prior nerve injury in rats that had developed continuous mechanical allodynia subsequent to sciatic cryoneurolysis (SCN). Allodynia was attenuated (thresholds increased) after administration of the alpha 1 antagonist prazosin, but not the alpha 2 antagonist idazoxan. Similar attenuation occurred with infusions of the alpha 2 agonist dexmedetomidine and at the lowest dose (2.0 micrograms) of the mixed alpha agonist clonidine. In contrast, allodynia was exacerbated (thresholds decreased) by infusion of the highest dose of clonidine (20 micrograms). Infusions of the alpha 2 Zocor 40mg Tablets agonist ST-91, a polar analog of clonidine, did not alter withdrawal thresholds. The findings suggest that a minimal peripheral adrenergic modulation of SCN-induced allodynia occurs via mechanisms that are not localized to the prior injury site. However, overall, the SCN model of neuropathic pain appears to be resistant to adrenergic interventions, providing further evidence that SCN in rats is a model of sympathetically independent pain (SIP).

minipress 1mg tablet 2017-10-29

This analysis examines the relative effectiveness of Clomid Fertility Medication current medical therapies for BPH in preventing AUR, AUR-related catheterisation and surgery in real-life clinical practice.

minipress xl drug 2015-08-22

Previously, we have reported that norepinephrine (NE)-mediated cardiac hypertrophy may occur due to stimulation of alpha1-adrenoceptors and phospholipase C (PLC) activity. Since the signal transduction mechanisms involving PLC isozymes in cardiomyocytes are not well established, the present study was conducted to test the hypothesis that stimulation of cardiac PLC activity by NE increases the gene expression for PLC isozymes via a PKC and ERK 1/2-dependent pathway. For this purpose, mRNA levels for PLC beta1, beta3, gamma1, and delta1 isozymes were determined in isolated adult rat cardiomyocytes upon incubation in the absence and presence of NE. The NE-induced Viagra Pill Splitting increases in PLC isozyme mRNA levels were not only attenuated by prazosin, an inhibitor of alpha1-adrenergic receptor, but also by U73122, an inhibitor of PLC activity. Alterations in NE-induced PLC gene expression by both prazosin and U73122 were associated with inhibition of PLC activity. The inhibition of NE-stimulated PLC gene expression by bisindolylmaleimide, a PKC inhibitor, and PD98059, an ERK1/2 inhibitor, indicated that PKC-MAPK signaling may be involved in this signal transduction pathway. The observed NE-induced changes in gene expression in the presence of different inhibitors were associated with corresponding changes in the protein content. Furthermore, significant increases in mRNA levels and protein contents for all PLC isozymes were found in cardiomyocytes treated with phorbol 12-myristate 13-acetate, a PKC activator. These data indicate that PLC isozymes may regulate their own gene expression through a PKC and ERK 1/2-dependent pathway in a cycle of events associated with the cardiomyocyte hypertrophic response.

minipress ptsd dosage 2016-08-18

We present here a long-term observation of 2 children with a rare syndrome with a non-neurogenic neurogenic bladder dysfunction (Hinman's syndrome), and we investigated the safety and efficacy of long-term use of terazosine in association with Asacol Prices Online prophylactic antibiotics, timed voiding and a bowel regimen.

minipress drug interactions 2015-04-02

Fragmentation of rapid eye movement sleep (REMS) is well described in individuals with posttraumatic stress disorder (PTSD) and likely has significant functional consequences. Fear-conditioned rodents may offer an attractive model of the changes in sleep that characterize PTSD. Following fear conditioning (FC), Wistar-Kyoto (WKY) rats, a strain known to be particularly stress-sensitive, have increased REMS fragmentation that can be quantified as a shift in the distribution of REMS episodes towards the more frequent occurrence of sequential REMS (inter-REMS episode interval≤3 min) vs. single REMS (interval>3 min). The α1 adrenoceptor antagonist prazosin has demonstrated efficacy in normalizing sleep in PTSD. To determine the utility of fear-conditioned WKY rats as a model of sleep disturbances typical of PTSD and as a platform for the development of new treatments, we tested the hypothesis that prazosin would reduce REMS fragmentation in fear-conditioned WKY rats. Sleep parameters and freezing (a standard measure of anxiety in rodents) were quantified at baseline and on Days 1, 7, and 14 following FC, with either prazosin (0.01mg/kg, i.p.) or vehicle injections administered prior to testing in a between-group design. Fear conditioning was achieved by pairing tones with Combivir Medicine a mild electric foot shock (1.0mA, 0.5s). One, 7, and 14 days following FC, prazosin or vehicle was injected, the tone was presented, freezing was measured, and then sleep was recorded from 11 AM to 3 PM. WKY rats given prazosin, compared to those given vehicle, had a lower amount of seq-REMS relative to total REMS time 14 days after FC. They also had a shorter non-REMS latency and fewer non-REMS arousals at baseline and on Days 1 and 7 after FC. Thus, in FC rats, prazosin reduced both REMS fragmentation and non-REMS discontinuity.

minipress capsules 2015-09-23

Strips of vas deferens were suspended in an organ bath and Zantac Yellow Pill subjected to electrical stimulation to establish frequency-response curves. These stimulations were repeated in the presence of pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, P2 receptor antagonist), prazosin (adrenergic alpha1 antagonist), and tetrodotoxin. Concentration-response curves were constructed to noradrenaline and the P2X agonists ATP and alpha,beta-methylene ATP (alpha,beta-meATP). The P2X receptor subtype distribution was assessed by immunohistochemistry using specific antibodies.

minipress reviews 2015-09-22

The effect of alpha 2-adrenergic receptor activation on adenylate cyclase activity in Chinese hamster ovary cells stably transfected with the alpha 2A-adrenergic receptor gene is biphasic. At lower concentrations of epinephrine forskolin-stimulated cyclic AMP production is inhibited, but at higher concentrations the inhibition is reversed. Both of these effects are blocked by the alpha 2 antagonist yohimbine but not by the alpha 1 antagonist prazosin. Pretreatment with pertussis toxin attenuates inhibition at lower concentrations of epinephrine and greatly potentiates forskolin-stimulated cyclic AMP production at higher concentrations of epinephrine. alpha 2-Adrenergic receptor stimulation also causes arachidonic acid mobilization, presumably via phospholipase A2. This effect is blocked Epivir Syrup by yohimbine, quinacrine, removal of extracellular Ca2+, and pretreatment with pertussis toxin. Quinacrine and removal of extracellular Ca2+, in contrast, have no effect on the enhanced forskolin-stimulated cyclic AMP production. Thus, it appears that the alpha 2-adrenergic receptor in these cells can simultaneously activate distinct signal transduction systems; inhibition of adenylate cyclase and stimulation of phospholipase A2, both via G1, and potentiation of cyclic AMP production by a different (pertussis toxin-insensitive) mechanism.

minipress user reviews 2017-04-17

Oxaliplatin (4mg/kg) was administered intraperitoneally twice a week for 4weeks. Cold hyperalgesia was assessed Urispas Tablet Usage using the acetone test and mechanical allodynia was evaluated using the von Frey test.