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Results for “Adrenergic beta-Antagonists”

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At least 19 recordsLinked to original sources
PubMed1979

Direct binding studies of adrenergic receptors: biochemical, physiologic, and clinical implications.

Recently developed radioligand binding techniques permit direct investigation of the alpha- and beta-adrenergic receptors for catecholamines in a wide variety of tissues. These techniques allow the receptors to be quantitated, characterized, and studied under varying conditions of physiologic and pathophysiologic interest. They are providing fresh insights into the mechanisms by which endogenous catecholamines and other hormones regulate the properties of the adrenergic receptors and, in turn, control tissue sensitivity to catecholamine action.

Adrenergic alpha-Agonists↗
PubMed1977

Prazosin-new hypertensive agent. A double-blind crossover study in the treatment of hypertension.

Prazosin hydrochloride, a new antihypertensive agent, is said to be of mild-to-moderate potency when used as a sole agent in mild-to-moderate hypertension and when used in conjunction with other agents in severe hypertension. In our study of 14 patients comparing hydrochlorothiazide with prazosin, the antigypertensive effect of prazosin was less than that of hydrochlorothiazide. The greatest application of prazosin may be in conjunction with thiazide diuretics and beta-adrenergic blocking agents as the second or third drug.

Adrenergic beta-Antagonists↗
PubMed2026

The role of adjunctive aqueous suppressants for anti-vascular endothelial growth factor therapy: A systematic review.

Our goal is to determine whether adjunctive aqueous suppressants (topical β-blockers, carbonic anhydrase inhibitors, or oral acetazolamide) enhance outcomes of anti-vascular endothelial growth factor (anti-VEGF) therapy for diabetic macular edema (DME), retinal vein occlusion (RVO), and neovascular age-related macular degeneration (nAMD), focusing on retinal thickness, visual acuity, injection burden, intraocular pressure (IOP), and safety. DME, RVO, and nAMD are leading causes of vision loss treated with repeated intravitreal injections, yet many eyes show persistent fluid. Aqueous suppressants are inexpensive and widely available, with potential to prolong intravitreal drug residence and improve outcomes, but their clinical value remains uncertain. Following a registered protocol, we searched 4 databases (January, 2000 toMay, 2025) for randomized and comparative studies evaluating adjunct aqueous suppressants with anti-VEGF therapy. Primary outcome was change in retinal thickness; secondary outcomes included visual acuity, injection burden, IOP, and adverse events. Risk of bias was assessed and findings synthesized narratively. Twelve studies (7 randomized trials; 495 eyes) met inclusion criteria. In DME, 3 of 4 trials showed greater thickness reduction with adjunctive dorzolamide (±timolol), although visual gains were inconsistent. In RVO, 1 trial suggested transient anatomical benefit, whereas oral acetazolamide showed no added effect. In nAMD, adjunctive dorzolamide-timolol reduced residual fluid in refractory cases without visual or treatment-sparing benefit. Topical therapy produced modest IOP reductions without serious adverse events. Adjunct aqueous suppressants may provide limited short-term anatomical benefit, particularly in DME and refractory nAMD, but consistent functional or durability effects are not found in this study. Larger, longer-term randomized studies are needed.

Humans↗
PubMed2026

Catecholaminergic polymorphic ventricular tachycardia mediated by ryanodine receptor 2: a validated risk stratification.

BACKGROUND AND AIMS: Patients with catecholaminergic polymorphic ventricular tachycardia (CPVT) are at risk for potentially life-threatening arrhythmic events (AEs) even while treated with β-blockers. The aim was to develop a model for individualized prediction of AEs in patients with RYR2-mediated CPVT on β-blocker monotherapy. METHODS: The derivation and independent validation cohorts included 743 and 129 patients, respectively. AEs were defined as arrhythmic syncope, appropriate implantable cardioverter-defibrillator shock, sudden cardiac arrest (SCA), and sudden cardiac death. Near-fatal or fatal AEs (nf/fAEs) included all AEs except for arrhythmic syncope. Prediction models using Cox regression were developed and internally and externally validated. RESULTS: A total of 102 (13.7%) patients in the derivation cohort and 24 (18.6%) patients in the validation cohort experienced ≥1 AE over a median follow-up of 5.1 [interquartile range (IQR), 7.7] and 2.4 (IQR, 4.4) years, respectively. Predictors of AE were arrhythmic syncope or SCA prior to diagnosis and age at β-blocker initiation. In the derivation and validation cohorts, the optimism-corrected C-indices of the models for AE were 0.67 [95% confidence interval (CI) 0.62-0.72] and 0.59 (95% CI 0.48-0.71), respectively. For nf/fAEs, ventricular arrhythmia severity before β-blocker initiation was a fourth independent predictor, and C-indices of the models in the derivation and validation cohorts were 0.74 (95% CI 0.68-0.80) and 0.60 (95% CI 0.47-0.72), respectively. In the derivation cohort, calibration slopes were 1.00 (95% CI 0.59-1.41) for AE and 1.00 (95% CI 0.69-1.32) for nf/fAE. CONCLUSIONS: These externally validated risk prediction models using clinical parameters accurately distinguished CPVT patients on β-blocker monotherapy at low and high risk for future AEs while treated with β-blockers. These models provide guidance for implementation of clinical management therapies to prevent AEs in patients with CPVT.

Humans↗
PubMed1976

Raynaud's phenomenon as side effect of beta-blockers in hypertension.

A series of 102 hypertensive patients were assessed for the frequency of symptoms of Raynaud's phenomenon and absent peripheral pulses. Out of 21 patients receiving methyldopa alone only one had cold hands and feet whereas among patients on beta-blockers the incidence was 50%. The frequency of both symptoms and absent pulses was highest in patients taking propranolol compared with those taking atenolol or oxprenolol. Patients without a foot pulse were much more likely to have cold hands. A change from propranolol to oxprenolol in some symptomatic patients resulted in improvement. In two patients the skin temperature fell after an 80-mg dose of propranolol. The mechanism by which beta-blockers induce Raynaud's phenomenon is still not clear.

Adrenergic beta-Antagonists↗
PubMed1977

Observations in man of hypoglycaemia during selective and non-selective beta-blockade.

The acute hypoglycaemic reaction is accompanied by a rise in systolic and a slight fall in diastolic blood pressure and a tachycardia. In contrast, during beta-blockade with propranolol there is a rise of both systolic and diastolic blood pressures and bradycardia. Restoration of blood glucose to normal is delayed. With metoprolol there is a lesser increase in diastolic blood pressure and a slight tachycardia. Restoration of the blood glucose to normal is little delayed. When patients liable to hypoglycaemia require a beta-blocking agent, it is suggested that a selective blocker such as metoprolol should be used.

Acute Disease↗
PubMed1975

Effects of several beta-blockers on blood pressure in the rat.

Effects of practolol, alprenolol and pindolol on blood pressure in the rat were studied. Also effects of these three beta-blocking agents on blood pressure and heart rate in spinal rats during adrenaline infusion were studied and compared with those of propranolol. The beta-blocking agents produced a sustained pressor action in the rat, and in the spinal rat infused with adrenaline. The magnitude of the pressor action induced by the beta-blockers was in the following order: pindolol larger than or equal to propranolol larger than or equal to alprenolol greater than practolol. Minimum doses of these beta-blockers required to cause a pressor action in the spinal rat infused with adrenaline were in the following order; practolol greater than alprenolol larger than or equal to propranolol larger than or equal to pindolol. The magnitude of the pressor action produced by the same dose of these beta-blockers and minimum doses of these beta-blockers required to cause a pressor action in the spinal rat infused with adrenaline seemed to be roughly proportional to their beta-receptor blocking activities. It was concluded that the minimum doses of these beta-blockers required to cause a pressor action and the magnitude of the pressor action induced by the beta-blockers in the spinal rat infused with adrenaline could be used to compare their beta-blocking activities and that practolol, a cardioselective beta-blocker, seems to block not only cardiac beta-receptor but to some extent also peripheral vascular beta-receptors.

Adrenergic beta-Antagonists↗
PubMed1976

The difficult hypertensive.

With the wide range of medications available today it should be possible to obtain satisfactory control in the majority of hypertensive patients. However, there are various categories of patients who may present particular problems in management, as for example patients with cerebro-vascular and coronary disease, or with renal failure. A particularly important group is those presenting with severe resistant hypertension, and these patients may constitute about 5 to 10% of the hypertensive population. Considerations relevant to the management of patients presenting with such problems are discussed. Combined drug regimens employing clonidine or beta-blockers with peripheral vasodilators appear to be particularly useful.

Adrenergic beta-Antagonists↗
PubMed1977

[Treatment of ischemic heart disease with "coronary drugs" (author's transl)].

The standard treatment of ischemic heart disease consists in the administration of nitrates and beta-sympathicolytic agents. Calcium antagonists are likewise promising. They should be used particularly if beta-sympathicolytic agents are contraindicated. In the beginning special caution should be exercised on combining a beta-sympathicolytic agent with a calcium antagonist. This is best done under clinical supervision since sudden cardiac decompensation, extreme bradycardia and/or disturbed atrioventricular conduction is to be expected. Today the administration of "coronary dilators" is no longer a part of the standard treatment but can at best be regarded as supplementary therapy.

Adrenergic beta-Antagonists↗
PubMed1976

Sympathetic cardiovascular effects of experimental strychnine poisoning in dogs.

The cardiovascular effects of intravenously administered strychnine were studied in anesthetized and paralyzed dogs. Administration of strychnine in cumulative doses of up to 0.1 to 0.2 mg/kg caused significant pressor, as well as positive inotropic and chronotropic, effects on the heart which were abolished by adrenergic blocking agents. The cardiovascular responses possibly were elicited by a central mechanism in contrast to the peripheral inhibitory action of strychnine on the sympathetic system. Diazepam caused a marked attenuation of the pressor response with only slight changes on the heart. A combination of diazepam and propranolol would appear to be a useful therapy in cases of strychnine poisoning showing marked cardiovascular excitation.

Adrenergic alpha-Antagonists↗
PubMed1975

Treatment of renal hypertension.

There are different types of renal hypertension: hypertension due to parenchymal renal disease, renovascular hypertension, hypertension due to urological disease, hypertension of endstage renal disease. Treatment has to consider-above all-the possibility of specific, medical or surgical procedures that may cause the underlying condition. If the underlying disease is not amenable to specific therapy, symptomatic medical treatment to lower blood pressure is indicated: besides control of sodium-intake and body weight antihypertensive drugs are generally indicated. We use them, alone or in combination, in the following line of order: diuretics, beta-adrenergic blockers, dihydralazine, reserpine, clonidine, alpha-methyldopa, guanethidine.

Adrenergic beta-Antagonists↗
PubMed1977

[Treatment of coronary insufficiency with beta-receptor antagonists (author's transl)].

The pathophysiology of the coronary insufficiency, the effect of beta-receptor antagonists, the understanding of these effects on the basis of the pathophysiology and the possibilities of testing beta-receptor antagonists in patients with coronary insufficiency are discussed. It is pointed out that the pathophysiology of the coronary insufficiency is based on the difference between oxygen demand of and oxygen supply to the myocardium. beta-Receptor antagonists compensate for this difference. Testing beta-receptor antagonists should include tolerance to exercise and controlled studies using standard medication for comparison.

Adrenergic beta-Antagonists↗