minipress 2 mg
Currently available data and clinical observations which suggest that there is a pathogenetic relationship between hypertension, diabetes mellitus, and atherosclerosis have provided a concept of the X syndrome, by which hypertensive patients, mainly males, have impaired insulin tolerance along with hyperinsulinemia and concurrent atherogenic disorders of lipid metabolism. The paper discussed the specific pathogenetic mechanisms, clinical manifestations, and prospects for drug correction of the metabolic syndrome. The treatment of arterial hypertension with the calcium antagonist Lomir has indicated there are no negative changes as a control of non-insulin-dependent diabetes mellitus in the presence of effective correction of arterial hypertension and atherogenic dyslipidemias. With the monotherapy of essential hypertension concurrent with hypercholesterolemia with the alpha 1-adrenoblocker Doxazosin, in addition to the agent's high antihypertensive effects, the authors noted its favourable action on lipid spectral parameters and platelet functional activity. There is abundant evidence for the use of specific hypolipidemic agents in patients with essential hypertensive refractory to current antihypertensive drugs. The data obtained with the use of Lescol (fluvastatin) in patients with hypertensive disease and hypercholesterolemia suggest that by substantially reducing the levels of total cholesterol, triglycerides, low density lipoprotein cholesterol and its transport protein apo B does not deteriorate the quality of correction of arterial hypertension in this group of patients.
Our data suggest that the vascular response to chronic stress is an adaptation to its deleterious effects, such as hypertension. In addition, this adaptation is NO- and Ca(2+)-dependent. These data help to clarify the contribution of stress to cardiovascular abnormalities. However, further studies are necessary to better elucidate the mechanisms involved in the cardiovascular dysfunction associated with stressors.
Blockade of alpha(1)-adrenoreceptors with prazosin produces bradycardia. The degree of this bradycardia in rats depends on age. In adult (20-week-old) rats bradycardia is pronounced, in 3-week-old rats it is insignificant, and in 1-week-old rats bradycardia does not develop. Prazosin moderates bradycardia induced by vagal stimulation in rats of different age.
minipress max dose
Growth of capillaries in the heart occurs under physiological circumstances during endurance exercise training, exposure to high altitude and/or cold, and changes in cardiac metabolism or heart rate elicited by modification of thyroid hormone levels. Capillary growth in all these conditions can be linked with increased coronary blood flow, decreased heart rate, or both. This paper brings evidence that, although increased blood flow due to long-term administration of coronary vasodilators results in capillary growth, a long-term decrease in heart rate induced by electrical bradycardial pacing in rabbits and pigs, or by chronic administration of a bradycardic drug, alinidine, in rats, stimulates capillary growth with little or no change in coronary blood flow. Decreased heart rate results in increased capillary wall tension, increased end-diastolic volume and increased force of contraction, and thus stretch of the capillary wall. This could lead to release of various growth factors possibly stored in the capillary basement membrane. Correlation was found between capillary density (CD) and the levels of low molecular endothelial cell stimulating angiogenic factor (ESAF) both in rabbit and pig hearts with CD increased by pacing. There was no relation between expression of mRNA for basic fibroblast growth factor and CD in sham-operated and paced rabbit hearts. In contrast, mRNA for TGF beta was increased in paced hearts, and the possible role of this factor in the regulation of capillary growth induced by bradycardia is discussed.
Lidamidine, a new antidiarrheal agent, produced a dose-dependent increase in plasma glucose levels in fed rats. The hyperglycemic response was evident 10 min after oral administration of lidamidine and lasted for 4 hr. Lidamidine's effect was absent in alloxanized rats. Insulin administration prevented the hyperglycemia. Pretreatment with the alpha 2-adrenoceptor antagonists yohimbine or RX781094A blocked the hyperglycemic response, while prazosin, propranolol, and hexamethonium pretreatment had no effect. These results indicate that the hyperglycemic effect of lidamidine is primarily due to the activation of peripherally located alpha 2-adrenoceptors that inhibit the release of insulin from pancreatic beta-cells.
minipress drug class
The S(-)PRO stimulus was shown to be centrally mediated, dose-related, time dependent, and stereoselective: S(-)PRO (ED(50) = 2.2 mg/kg) was twice as potent as (+/-)PRO and approximately four times as potent as R(+)PRO. The S(-)PRO stimulus generalized fully to the beta-adrenoceptor agent pindolol, the alpha(1)-adrenoceptor agonist methoxamine, cocaine, and the serotonergic agents TFMPP and RU 24969; partial generalization occurred to (-)ephedrine and nisoxetine but not to fenfluramine or 5-OMe DMT. The S(-)PRO stimulus was blocked completely (and competitively) when prazosin, an alpha(1)-adrenoceptor antagonist, was given in combination with the training dose of S(-)PRO. Moreover, prazosin exerted antagonism of the S(-)PRO-like effect of (+/-)PRO or R(+)PRO but produced only partial antagonism of the S(-)PRO-like effect of cocaine. In a second study, rats were trained to discriminate 8 mg/kg of cocaine from saline. The cocaine stimulus generalized to S(-)PRO, (+/-)PRO, and R(+)PRO. Prazosin partially attenuated the stimulus effect of cocaine (8 mg/kg) but completely blocked the cocaine-like effects of (+/-), S(-), and R(+)PRO.
tab minipress dose
Substantial evidence indicates that brain neurons containing and secreting norepinephrine (NE) and corticotrophin-releasing hormone (CRH) are activated during stress. The acoustic startle reflex (ASR) can be enhanced by CRH neuronal activity in the central nucleus of the amygdala. Our previous study demonstrates an augmentation of the footshock-induced ASR (f-ASR) 1 day after chronic variable stress (CVS) for 13 days. In this study, to evaluate a long-term neural plasticity in NE-CRH systems after CVS, we examined f-ASR 1, 8 or 15 days after CVS. The augmented magnitude of the f-ASR 15 day after CVS was potentiated and delayed compared with that 1 day after CVS. The delayed augmentation of f-ASR was inhibited by repeated treatment with desipramine, maprotiline or paroxetine for 14 days after CVS. A single treatment with any antidepressant agent had no influence the f-ASR while a marked inhibition by a single dose of alprazolam, CRH1-receptor antagonist, prazosin and propranolol was observed. The decreased tyrosine hydroxylase activity in the locus coeruleus and the beta-adrenoceptor down-regulation in the amygdaloid complex might be involved in the inhibiton of the delayed augmentation of f-ASR by repeated antidepressant treatment, leading to the possibility that the delayed sensitization of CRH response to stress after CVS might contribute to the biological mechanism underlying the formation of pathological states such as anxiety and depressive disorders.
minipress xl dose
Forty-five patients diagnosed as having BPH and clinically diagnosed micturition disorders were entered in a therapeutic protocol. Twenty-five patients received Prazosin and the remaining 20 patients were treated with Serenoa Repens for a period of 12 weeks. The symptomatology was assessed by flowmetry and the patients were questioned as to the irritative symptoms. It can be concluded from the study that Prazosin is slightly more effective in controlling the irritative symptoms produced by BPH.
minipress 6 mg
To examine the mechanism of the alpha 1-adrenoceptor-mediated inhibition of the release of thyroid hormones in the mouse thyroid, the effect of noradrenaline on the production of inositol phosphates was investigated using thyroids preloaded with [3H]inositol. Noradrenaline increased [3H]inositol accumulation into inositol phosphates in the mouse thyroid during a 30-min incubation whereas TSH (10 mU/ml) was without effect. The effect of noradrenaline was mimicked by phenylephrine, but not by clonidine or isoprenaline. Prazosin antagonized the effect of noradrenaline, while yohimbine had no effect. These results suggest that noradrenaline-induced production of inositol phosphates is mediated by alpha 1-adrenoceptors. The inhibition of release of thyroid hormones elicited by alpha 1-adrenergic agonists in the mouse thyroid is possibly mediated through the hydrolysis of membrane phosphoinositides followed by the generation of second messengers such as inositol phosphates and diacylglycerol.
minipress dosage forms
Positive chronotropic responses of rat isolated atria to phenylephrine were reduced by propranolol (0.3 microM) and the residual response was further depressed by the selective alpha 1-adrenoceptor antagonist prazosin (1 nM) but not yohimbine (10 nM), confirming that a component of the response to phenylephrine was due to activation of alpha 1-adrenoceptors. When beta-adrenoceptors were blocked by propranolol, the positive chronotropic response to phenylephrine was enhanced by increasing the calcium concentration and by the calcium channel activator Bay K 8644 (0.1 microM), whereas the response was decreased by lowering the calcium concentration and by the calcium antagonists verapamil (10 nM), nifedipine (10 nM) and diltiazem (100 nM). In the presence of prazosin, when phenylephrine acts only on beta-adrenoceptors, calcium antagonists had no effect on the response. In rat isolated aortic strips in a calcium-free, high K+ (40 mM) solution, verapamil (10 nM), nifedipine (10 nM) and diltiazem (100 nM) shifted the calcium-induced contraction curves to the right, but prazosin (10 nM) had no effect, indicating that it is not a calcium antagonist. The calcium antagonists in the concentrations stated above had no effect on phenylephrine-induced contractions of rat aortic strips in normal Krebs-Henseleit solution, indicating that they did not block alpha 1-adrenoceptors in these concentrations. Taken together, these data suggest that the positive chronotropic effect of phenylephrine resulting from activation of alpha 1-adrenoceptors involves an increased influx of calcium through channels that are sensitive to organic calcium antagonists.
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The aim was to study contractile responses of segments of rat arteries taken from pressure loaded and pressure protected regions and to examine the role of endothelial derived factors on the spontaneous activity of pressure loaded ring segments.