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Journal of Pharmacology And Experimental Therapeutics, Vol. 181, Issue 3, 425-433, 1972
Copyright © 1972 by American Society for Pharmacology and Experimental Therapeutics

THE PREVENTION OF ISOPROTERENOL DESENSITIZATION AND ISOPROTERENOL REVERSAL

JEROME H. FLEISCH 1 and ELWOOD TITUS 1

1 Laboratory of Chemical Pharmacology, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland

Relaxations of aortic smooth muscle to repeatedly applied high concentrations of isoproterenol were tachyphylactic (desensitization) and usually changed into contractions (isoproterenol reversal). Isoproterenol-induced contractions, however, were not tachyphylactic. Thus, the beta receptor action of isoproterenol can undergo densensitization whereas the action mediated by alpha receptors is resistant. Phentolamine, bromolysergic acid diethylamide, aminophylline, caffeine, theobromine, tetracaine, papavenine and nitroglycerin inhibited isoproterenol tachyphylaxis (desensitization) and prevented isoproterenol reversal. In addition, these compounds altered a previously established tachyphylaxis by converting the isoproterenol-induced contractions into relaxations. All of these agents were shown to inhibit alpha receptor mediated contractions but no correlation could be made between this action and their ability to prevent isoproterenol desensitization. Unlike aortic tissue, tracheal smooth muscle was not easily desensitized by isopnoterenol. Since none of the agents which prevent isoproterenol desensitization appear to interact with the beta receptor per se, it is postulated that this diverse group of organic substances interacts with the smooth muscle membrane in some manner which permits the beta adrenergic receptor system of aortic tissue to function without undergoing desensitization.

Submitted on December 20, 1971
Accepted on March 3, 1972




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Copyright © 1972 by the American Society for Pharmacology and Experimental Therapeutics.