RT Journal Article
SR Electronic
T1 BLOCKADE OF EPINEPHRINE-INDUCED HYPERGLYCEMIA
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 363
OP 376
VO 104
IS 3
A1 Harvey, Stewart C.
A1 Wang, C. Y.
A1 Nickerson, Mark
YR 1952
UL http://jpet.aspetjournals.org/content/104/3/363.abstract
AB 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 β-haloalkylamine (SKF 688A) was shown to suppress epinephrine-induced glycogenolysis in vitro at concentrations comparable to those effective in vivo.