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The contribution of renal and extrarenal mechanisms to hypokalemia induced by glucagon.

Abstract
Other investigators have shown that infusion of glucagon causes the concentration of potassium, [K+], in the arterial plasma to increase rapidly, then to decrease to less than the beginning value. In studies on anesthetized dogs, we found that the magnitude of the initial, rapid rise of [K+] was increased by nephrectomy but not affected by pancreatectomy. The subsequent decline of [K+] and the persistent hypokalemia were not affected significantly by nephrectomy. Plasma [K+] decreased in the nephrectomized-pancreatectomized dogs, as it did in the nephrectomized and the control groups, but the effect was temporary, and [K+] began to increase again, even though the infusion of glucagon continued; after the infusion was ended, plasma [K+] became significantly higher than the beginning value. These data suggest that the hypokalemia caused by infusion of glucagon initally depends on extrarenal factors other than insulin, and, later, depends on insulin.
AuthorsG W Pettit, R L Vick, M D Kastello
JournalEuropean journal of pharmacology (Eur J Pharmacol) Vol. 41 Issue 4 Pg. 437-41 (Feb 21 1977) ISSN: 0014-2999 [Print] Netherlands
PMID844485 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Insulin
  • Glucagon
Topics
  • Animals
  • Dogs
  • Female
  • Glucagon
  • Half-Life
  • Hypokalemia (chemically induced, physiopathology)
  • Insulin (metabolism)
  • Kidney (physiology)
  • Male
  • Pancreas (physiology)
  • Spleen (physiology)
  • Time Factors

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