Modification by beta-adrenergic blockade of the circulatory respones to acute hypoxia in man.
In 17 healthy men, beta-adrenergic blockade reduced significantly the tachycardia and the elevation of cardiac output associated with inhalation of 7.5% oxygen for 7 to 10 minutes. Hypoxia did not increase plasma concentrations of epinephrine or norepinephrine in six subjects. Furthermore, blockade of alpha and beta receptors in the forearm did not modify the vasodilation in the forearm induced by hypoxia, providing pharmacologic evidence that hypoxia of the degree and duration used was not associated with an increase in the concentrations of circulating catecholamines in man. Part of the increase in cardiac output and heart rate during acute hypoxia in man is produced by stimulation of beta-adrenergic receptors, probably by cardiac sympathetic nerves. The mechanism of the vasodilation in the forearm during hypoxia remains uncertain.
D000328:Adult; D001775:Blood Circulation; D001783:Blood Flow Velocity; D001795:Blood Pressure Determination; D002302:Cardiac Output / Q000187:drug effects*; D004837:Epinephrine / Q000097:blood*; D004983:Ethanolamines / Q000494:pharmacology; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000097:blood*; D010100:Oxygen / Q000494:pharmacology; D010643:Phenoxybenzamine / Q000494:pharmacology; D011311:Pressoreceptors / Q000502:physiology; D013610:Tachycardia / Q000188:drug therapy*
D004983:Ethanolamines; D010643:Phenoxybenzamine; D010100:Oxygen; D009638:Norepinephrine; D004837:Epinephrine