Journal ArticleDOI
Elevated beta-adrenergic receptor number after chronic propranolol treatment.
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TLDR
Findings may represent the converse of agonist-induced desensitization which is associated with decreases in beta-receptor number and provide a potential explanation for the clinically observed “propranolol withdrawal syndrome”.About:
This article is published in Biochemical and Biophysical Research Communications.The article was published on 1977-09-23. It has received 255 citations till now. The article focuses on the topics: Propranolol & Dihydroalprenolol.read more
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Mechanisms of membrane-receptor regulation. Biochemical, physiological, and clinical insights derived from studies of the adrenergic receptors.
TL;DR: Hormones and drugs initiate their biologic actions by binding to specific cellular recognition sites, termed receptors, and are followed by alterations of cellular metabol...
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Radioligand binding studies of adrenergic receptors: new insights into molecular and physiological regulation.
TL;DR: This article has focused on studies that provide new insights into factors that appear to regulate the function of the adrenergic receptors, either at a physiological or biochemical level, and has deliberately chosen several areas for more extensive coverage.
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Elevation of beta-adrenergic receptor density in human lymphocytes after propranolol administration.
TL;DR: Data show that propranolol administration leads to an increase in the density of beta-adrenergic receptors in human tissue, consistent with the hypothesis that some of the untoward effects observed after abrupt discontinuation of proPRanolol are caused by beta-receptor-mediated adrenergic hypersensitivity.
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Cardiovascular and Metabolic Alterations in Mice Lacking Both β1- and β2-Adrenergic Receptors
TL;DR: Genetic knockout models are utilized to test directly the role of β1- and/or β2-AR expression on homeostatic control mechanisms and suggest that in the mouse, β-AR stimulation of cardiac inotropy and chronotropy is mediated almost exclusively by theβ1-AR, whereas vascular relaxation and metabolic rate are controlled by all three β- ARs.
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Regulation of Human Leukocyte Beta Receptors by Endogenous Catecholamines: RELATIONSHIP OF LEUKOCYTE BETA RECEPTOR DENSITY TO THE CARDIAC SENSITIVITY TO ISOPROTERENOL
TL;DR: It is suggested that physiological levels of catecholamines normally down-regulate beta receptors in man and that blockade of this down-regulation by propranolol allows receptor density to increase.
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The Attractions of Proteins for Small Molecules and Ions
TL;DR: The number and variety of known compounrjs between proteins and small molecules are increasing rapidly and make a fascinating story as discussed by the authors, and there are many compounds of serum albumin, which was used during the war by many chemists, most of whom found at least one 6ew compound.
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Thyroid hormone regulation of beta-adrenergic receptor number.
TL;DR: It is demonstrated that thyroid hormones can regulate the number of cardiac beta-adrenergic receptors, and may be responsible, at least in part, for the enhanced catecholamine sensitivity of beta- adrenergic-coupled cardiac responses in the hyperthyroid state.
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beta-Adrenergic receptor involvement in 6-hydroxydopamine-induced supersensitivity in rat cerebral cortex.
TL;DR: The results suggest that changes in the density of adrenergic receptors are involved in 6-hydroxydopamine-induced supersensitivity at central noradrenergic synapses.
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Coronary Artery Syndromes After Sudden Propranolol Withdrawal
TL;DR: Six patients with stable exertional angina pectoris immediately developed unstable angina after cessation of propranolol therapy and the character and frequency of the pain episodes wereSignificant differences were found between patients with and without stable angina.