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Alpha Adrenergic Antagonist

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2501. Effect of alpha-adrenergic blockers, ACE inhibitors, and calcium channel antagonists on renal function in hypertensive non-insulin-dependent diabetic patients. (PubMed)

Effect of alpha-adrenergic blockers, ACE inhibitors, and calcium channel antagonists on renal function in hypertensive non-insulin-dependent diabetic patients. In the present study we investigated the effect of a selective alpha 1-adrenergic blocker (doxazosin), an angiotensin-converting enzyme (ACE) inhibitor (captopril), and a calcium channel antagonist (nifedipine) on renal function in hypertensive non-insulin-dependent diabetic patients. 30 NIDD hypertensive patients (age = 50 +/- 3 years (...) ), and nifedipine (155 +/- 4/93 +/- 1) groups prior to the start of antihypertensive therapy and declined to 143 +/- 3/84 +/- 3 (doxazosin), 139 +/- 3/82 +/- 3 (captopril), and 141 +/- 3/84 +/- 1 (nifedipine) mm Hg (all p < 0.01 vs. pretreatment). In summary, both doxazosin and captopril treatment were associated with significant rises in GFR, while all three antihypertensive agents caused a significant decline in proteinuria. These results indicate that alpha-adrenergic blockers, ACE inhibitors, and calcium

1996 Nephron

2502. Assessment of MK-467, a peripheral alpha 2-adrenergic receptor antagonist, with intravenous clonidine. (PubMed)

Assessment of MK-467, a peripheral alpha 2-adrenergic receptor antagonist, with intravenous clonidine. The activity of MK-467, a new peripherally acting alpha 2-antagonist, was assessed in volunteers by a randomized, double-blind, crossover design. One hour after administration of either 15 mg or 30 mg MK-467 or placebo, 200 micrograms clonidine was given intravenously and observations were made for a further 8 hours. Clonidine reduced plasma norepinephrine levels to 79% +/- 7 (...) than 0.05). Plasma insulin was suppressed by clonidine from 72 +/- 14 to 47 +/- 7 IU.L-1, an effect antagonised by both doses of MK-467 (p less than 0.05 in each case). MK-467 had no effect on clonidine-induced increased drowsiness, xerostomia, or increase in growth hormone secretion, which is consistent with it being a peripherally acting specific alpha 2-antagonist. The small effect of MK-467 on clonidine-induced changes in plasma glucose and insulin suggests that peripheral alpha 2-adrenergic

1991 Clinical pharmacology and therapeutics

2503. Reduction of hyperglycemia after oral glucose load by the new alpha 2-adrenergic receptor antagonist SL 84.0418 in healthy subjects. (PubMed)

Reduction of hyperglycemia after oral glucose load by the new alpha 2-adrenergic receptor antagonist SL 84.0418 in healthy subjects. To assess the antihyperglycemic activity of a new peripherally acting alpha 2-adrenergic receptor antagonist, SL 84.0418 in healthy volunteersThis was a randomized, double-blind crossover study. The effects of 10, 50, and 100 mg SL 84.0418 on blood glucose, plasma insulin, C-peptide, glucagon, epinephrine, and norepinephrine were investigated in comparison (...) and plasma norepinephrine increased during treatment with 50 and 100 mg SL 84.0418. Systolic and diastolic blood pressure were moderately enhanced by 50 and 100 mg SL 84.0418. Adverse effects reflecting alpha 2-adrenergic receptor blockade occurred more frequently with 100 mg SL 84.0418. The adverse effect profile of 50 mg SL 84.0418 was not different from that observed with glipizide.The alpha 2-adrenergic receptor antagonist SL 84.0418 dose dependently reduced the increase in blood glucose after

1994 Clinical pharmacology and therapeutics

2504. The inhibitory effect of a selective alpha 2-adrenergic receptor antagonist on moderate- to severe-type asthma. (PubMed)

The inhibitory effect of a selective alpha 2-adrenergic receptor antagonist on moderate- to severe-type asthma. Midaglizole (DG-5128), a novel selective alpha 2-adrenergic receptor antagonist, was administered to 17 patients with moderate to severe asthma in a single-dose, double-blind, randomized, crossover study. All patients also continued their regular treatment regimens. FEV1 increased significantly (p less than 0.05), and respiratory resistance decreased significantly (p less than 0.05 (...) ). Wheezing and dry rales on auscultation improved in patients receiving 200 mg of midaglizole, and their assessment of overall benefit was also significantly better (p less than 0.05). Blood pressure and heart rate were unaffected. However, plasma glucose levels fell slightly. This study demonstrated the bronchodilating effect of midaglizole in moderate to severe bronchial asthma. This selective alpha 2-adrenergic antagonist may prove to be a useful addition to current treatment regimens for asthma.

1989 The Journal of allergy and clinical immunology

2505. Effects of alpha- and beta-adrenergic antagonists on plasma apolipoproteins and forearm blood flow in patients with mild hypertension. (PubMed)

Effects of alpha- and beta-adrenergic antagonists on plasma apolipoproteins and forearm blood flow in patients with mild hypertension. To study the mechanisms by which adrenergic antagonists affect blood pressure and plasma lipid levels, the effects of alpha-blockade with prazosin were compared with those of beta-blockade with propranolol in 23 normolipidemic, mildly hypertensive patients. Plasma lipoprotein composition, apolipoproteins, and some of the processes involved in lipid synthesis (...) of plasma lipoproteins, measurements were taken of forearm blood flow, forearm vascular resistance, and maximal forearm vasodilatory potential during reactive hyperemia. The adrenergic antagonists had no effect on these measurements, nor did they affect cellular cholesterol synthesis as measured by the activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase in blood mononuclear cells. The results of this study demonstrate differing actions between alpha- and beta-adrenergic antagonism. Alpha

1989 The American journal of medicine

2506. [Platelet adrenergic alpha receptors in hypertensive subjects undergoing treatment with calcium antagonists]. (PubMed)

[Platelet adrenergic alpha receptors in hypertensive subjects undergoing treatment with calcium antagonists]. The effects of two different calcium-channel blocking agents on platelet alpha-2 adrenoceptors were studied in 18 mild to moderate hypertensive patients. The subjects were randomly assigned in a double blind fashion to treatment with either nifedipine 10 mg t.i.d. or tiapamil 300 b.i.d. for six weeks. Platelet alpha-2 receptors were studied before and following 6 weeks of treatment (...) using radioligand binding assay (3H Rauwolscine). Both agents induced a reduction in alpha-2 receptors, which reached statistical significance only for nifedipine. Such a reduction may contribute to the antihypertensive effect of calcium-channel blocking drugs.

1990 Bollettino della Società italiana di biologia sperimentale

2507. A pharmacodynamic study of the alpha 2-adrenergic receptor antagonist ethoxyidazoxan in healthy volunteers. (PubMed)

A pharmacodynamic study of the alpha 2-adrenergic receptor antagonist ethoxyidazoxan in healthy volunteers. Ethoxyidazoxan, a potent and highly selective alpha 2-adrenergic receptor antagonist, was administered intravenously to six healthy male volunteers in a double-blind, placebo-controlled, dose-rising design. Doses of 6 micrograms/kg and 8 micrograms/kg infused intravenously over 30 minutes produced significant elevations of plasma norepinephrine and body temperature and inhibited

1994 Clinical pharmacology and therapeutics

2508. Comparative effects of monatepil, a novel calcium antagonist with alpha 1-adrenergic-blocking activity, and nitrendipine on lipoprotein and carbohydrate metabolism in patients with hypertension. (PubMed)

Comparative effects of monatepil, a novel calcium antagonist with alpha 1-adrenergic-blocking activity, and nitrendipine on lipoprotein and carbohydrate metabolism in patients with hypertension. The effects of monatepil, a new calcium antagonist with alpha 1-blocking activity, and nitrendipine on lipoprotein and carbohydrate metabolism in 86 patients with mild-to-moderate hypertension were examined in a randomized, open-label, multicenter (32 hospitals) study. Thirty-nine patients treated (...) antagonist with favorable carbohydrate metabolism and lipid-lowering activity, although the clinical importance of these findings has not been established.

1994 American journal of hypertension

2509. Enhancement of morphine analgesia by the alpha 2-adrenergic antagonist yohimbine. (PubMed)

Enhancement of morphine analgesia by the alpha 2-adrenergic antagonist yohimbine. Although interactions between opioids and adrenergic agonists in the treatment of pain have been demonstrated in humans, the contribution of specific adrenergic receptors in this interaction remains to be clarified. In a double-blind, placebo-controlled study in male patients with postoperative dental pain, we investigated the effect of preoperative administration of the alpha 2-adrenergic antagonist, yohimbine (...) , on analgesia produced by postoperative intravenous morphine. Although yohimbine by itself did not affect the pain, the overall analgesic effect of morphine was significantly enhanced in the presence of yohimbine. This report is the first to demonstrate that an alpha 2-adrenergic antagonist enhances opiate analgesia in humans.

1995 Neuroscience

2510. Effect of the alpha 2-adrenergic antagonist yohimbine on orthostatic tolerance. (PubMed)

Effect of the alpha 2-adrenergic antagonist yohimbine on orthostatic tolerance. We studied the effect of yohimbine, a drug that inhibits presynaptic alpha 2-adrenergic receptors and increases the neuronal release of norepinephrine from the central and sympathetic nervous systems, on tolerance to cardiovascular stress in 10 untrained, healthy subjects. Using radioligand binding of tritiated yohimbine to platelets, these subjects were found to have a normal complement of alpha 2-adrenergic

1990 Hypertension

2511. Prokinetic effect of indoramin, an alpha-adrenergic antagonist, on human gall-bladder. (PubMed)

Prokinetic effect of indoramin, an alpha-adrenergic antagonist, on human gall-bladder. The effects of alpha- and beta-adrenergic agents on gall-bladder motility remain undefined.To determine the effects of alpha- and beta-antagonists on gall-bladder motility in healthy humans.In this single, blind, three-way crossover study, a slow-release formulation of propranolol 80 mg (beta-antagonist), indoramin 25 mg (post-synaptic alpha1-antagonist) and placebo were administered to 10 healthy volunteers (...) after the administration of propranolol was 17.49 +/- 2.37 mL and was not significantly different from placebo (16.50 +/- 2.78 mL). When the mean post-prandial gall-bladder volumes were compared, indoramin significantly enhanced post-prandial gall-bladder emptying compared to placebo (P < 0.001). There was no significant post-prandial volume difference between placebo and propranolol.Indoramin, an alpha-adrenergic antagonist, acts as a prokinetic agent, enhancing post-prandial gall-bladder emptying

2002 Alimentary pharmacology & therapeutics

2512. Effect on resting blood pressure and blood pressure homeostasis of short-term administration of the alpha 1-adrenergic receptor antagonist, trimazosin, in hypertension. (PubMed)

Effect on resting blood pressure and blood pressure homeostasis of short-term administration of the alpha 1-adrenergic receptor antagonist, trimazosin, in hypertension. The effects of trimazosin on blood pressure and cardiovascular homeostasis were studied in 12 subjects with untreated essential hypertension of mild or moderate degree. After a 3-day placebo period, the subjects were given trimazosin at the dose of 50, 100, or 200 mg twice daily (7 am and 7 pm) according to a randomized, double

1988 Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy

2513. Oral phentolamine: an alpha-1, alpha-2 adrenergic antagonist for the treatment of erectile dysfunction. (PubMed)

Oral phentolamine: an alpha-1, alpha-2 adrenergic antagonist for the treatment of erectile dysfunction. Phentolamine mesylate is an alpha-1 and alpha-2 selective adrenergic receptor antagonist which has undergone clinical trials for erectile dysfunction treatment. Biochemical and physiological studies in human erectile tissue have revealed a high affinity of phentolamine for alpha-1 and alpha-2 adrenergic receptors. Based on pharmacokinetic studies, it is suggested that 30-40 min following oral (...) ingestion of 40 or 80 mg of phentolamine (Vasomax), the mean plasma phentolamine concentrations are sufficient to occupy the alpha-1 and -2 adrenergic receptors in erectile tissue and thereby result in inhibition of adrenergic-mediated physiologic activity. In large multi-center, placebo-controlled pivotal phase III clinical trials, the mean change in the erectile function domain of the International Index of Erectile Function scores (Questions 1-5 and 15) from screening to the end of treatment

2000 International journal of impotence research

2514. Comparison between an alpha-adrenergic antagonist and a beta 2-adrenergic agonist in bronchial asthma. (PubMed)

Comparison between an alpha-adrenergic antagonist and a beta 2-adrenergic agonist in bronchial asthma. Fifteen patients suffering from asthma received inhalations of phentolamine, albuterol (salbutamol), a combination of phentolamine and albuterol, and placebo, in a single-blind fashion; the changes in the pulmonary function tests were recorded over a three-hour period. Three patients responded to phentolamine with marked bronchodilatation, whereas severe bronchoconstriction was induced (...) by the drug in two patients. Five patients improved more with phentolamine than with placebo, while all patients improved more markedly with albuterol and still more following inhalation of the combination of both drugs. As a group, there were no statistically significant differences between the responses to phentolamine compared with placebo, or between albuterol alone compared with the combination of both drugs. We concluded that both alpha-antagonist and beta 2-agonist agents act in the same direction

1983 Chest

2515. Clinical and physiological effects of an acute alpha-1 adrenergic agonist and a beta-1 adrenergic antagonist in chronic orthostatic intolerance. (PubMed)

Clinical and physiological effects of an acute alpha-1 adrenergic agonist and a beta-1 adrenergic antagonist in chronic orthostatic intolerance. Adrenergic agents are commonly used in the treatment of chronic orthostatic intolerance with postural tachycardia syndrome (POTS). POTS may be associated with increased limb blood flow ("high flow") and defective orthostatic vasoconstriction or decreased limb blood flow ("low flow") and potentially with small blood volume.We investigated (...) the consequences of short-term intravenous administration of an alpha-1 adrenergic agonist, phenylephrine, and a beta-1 adrenergic antagonist, esmolol, in 14 patients with POTS aged 13 to 19 years. Indices of heart rate and blood pressure variability, peripheral blood flow, and arterial resistance were assessed, and the capacitance relation was computed for every subject using venous occlusion plethysmography. Patients were tilted to 35 degrees upright while medicated and while unmedicated, and measurements

2002 Circulation

2516. Blockade of vasospastic attacks by alpha 2-adrenergic but not alpha 1-adrenergic antagonists in idiopathic Raynaud's disease. (PubMed)

Blockade of vasospastic attacks by alpha 2-adrenergic but not alpha 1-adrenergic antagonists in idiopathic Raynaud's disease. Idiopathic Raynaud's disease is characterized by cold-induced digital vasospasms, but its origin has not been established. Previous research has shown that peripheral vascular alpha 2-adrenergic receptors are hypersensitive to local cooling in these patients, but the role of alpha 1-adrenergic receptors is not clear. Moreover, the role of adrenergic receptors (...) in the production of actual vasospastic symptoms has not been investigated.We studied 23 patients with idiopathic Raynaud's disease who were screened using conservative criteria. They were randomly assigned to receive brachial artery infusions of an alpha 1-antagonist, an alpha 2-antagonist, or both while vasospastic attacks were induced by cooling in the laboratory. Each patient's hands were photographed, and the number of attacks in the infused hand was compared with the number in the contralateral hand

1995 Circulation

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