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Journal of Pharmacology And Experimental Therapeutics, Vol. 104, Issue 3, 363-376, 1952
Copyright © 1952 by American Society for Pharmacology and Experimental Therapeutics


BLOCKADE OF EPINEPHRINE-INDUCED HYPERGLYCEMIA

Stewart C. Harvey 1, C. Y. Wang 2, and Mark Nickerson 3

1 Department of Pharmacology, University of Utah College of Medicine, Salt Lake City, Utah
2 National Shanghai Medical College, Shanghai, China
3 Department of Pharmacology, University of Michigan School of Medicine, Ann Arbor, Michigan

1. Fifteen compounds were studied for their ability to suppress epinephrine-induced hyperglycemia and the pressor response to epinephrine in the rabbit and in the cat.

2. All fifteen compounds manifested some degree of suppression of the hyperglycemia. Thus this property seems to be common to all adrenergic blocking agents, as well as to a variety of agents which do not block other responses to epinephrine.

3. Suppression of epinephrine-induced hyperglycemia generally requires much higher doses of an adrenergic blocking agent than does suppression of epinephrine-induced pressor responses, especially in the cat. In general, smaller doses of each agent were required to suppress hyperglycemia in the rabbit than in the cat.

4. Ergonovine was found to have hyperglycemia-suppressing activity at doses having no apparent effect on cardiovascular responses to epinephrine.

5. No correlation was observed between the ability to suppress the hyperglycemia and the ability to suppress pressor responses. It seems likely, therefore, that the "hyperglycemia receptors" are different from the "pressor receptors" or that a completely different mechanism of action is involved in the suppression of these two responses.

6. A beta-haloalkylamine (SKF 688A) was shown to suppress epinephrine-induced glycogenolysis in vitro at concentrations comparable to those effective in vivo.

Submitted on December 3, 1951







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Copyright © 1952 by the American Society for Pharmacology and Experimental Therapeutics.