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Journal of Pharmacology And Experimental Therapeutics, Vol. 156, Issue 3, 452-462, 1967
Copyright © 1967 by American Society for Pharmacology and Experimental Therapeutics

A COMPARISON OF THE ADRENERGIC RECEPTOR BLOCKING PROPERTIES OF 1-(4'-METHYLPHENYL)-2-ISOPROPYLAMINO-PROPANOL-HCl AND PROPRANOLOL

Bernard Levy 1

1 Department of Pharmacology, University of Texas, Medical Branch, Galveston, Texas

The effects of 1-(4'-methylphenyl)-2-isopropylamino-propanol-HCl (H 35-25) treatment on a number of adrenergic responses to isoproterenol were determined in the anesthetized dog and the isolated rat uterus. H 35-25 was compared, quantitatively, to propranolol in the anesthetized dog studies. Studies in the dog included the effects of treatment with H 35-25 and propranolol, in a dose range of 0.1 to 3.0 mg/kg, upon the positive inotropic, positive chronotropic, vasodilator, blood pressure and intestinal inhibitory responses to isoproterenol. Studies with the isolated, spontaneously contracting rat uterus consisted of a determination of both the intrinsic action of H 35-25 and its ability to modify the rat uterine inhibitory response to isoproterenol. Propranolol blocked all of the responses to isoproterenol in the anesthetized dog, simultaneously, in the same dose range (0.1-1.0 mg/kg). H 35-25 produced a blockade of the vasodilator and blood pressure responses to isoproterenol in a dose range of 0.3 to 1.0 mg/kg but did not block the positive inotropic, positive chronotropic or intestinal inhibitory responses to isoproterenol. In the rat uterus, H 35-25 produced an intrinsic inhibitory response which was abolished by propranolol. H 35-25 was also capable of blocking the rat uterine inhibitory response to isoproterenol. H 35-25 appears to be capable of producing a selective blockade of vascular beta receptors in a dose range that has little blocking action on cardiac beta receptors.

Submitted on September 30, 1966
Accepted on January 16, 1967




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Copyright © 1967 by the American Society for Pharmacology and Experimental Therapeutics.