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AJP - Renal Physiology, Vol 249, Issue 2 319-F322, Copyright © 1985 by American Physiological Society
ARTICLES |
A. J. Premen
We ascertained the importance of the liver in mediating glucagon-induced increases in renal blood flow (RBF) and glomerular filtration rate (GFR) by comparing the renal hemodynamic responses to intrarenal versus intraportal infusion of glucagon at 3 ng X kg-1 X min-1 (a dose previously considered "physiologic") in two separate sets of anesthetized dogs. Following intrarenal infusion for 60 min (n = 6), glucagon was without effect on RBF and GFR. On the average, RBF and GFR increased by only 2 +/- 1 and 3 +/- 1%, respectively. However, in a second group of dogs (n = 6), intraportal infusion of glucagon significantly increased both RBF and GFR by the same order of magnitude over 60 min. RBF and GFR increased, on the average, by 22 +/- 2 and 20 +/- 2%, respectively. Peak responses occurred 30 min following glucagon infusion when RBF and GFR were elevated by 25 +/- 2 and 26 +/- 2%, respectively. In neither group of dogs were filtration fraction, arterial pressure, heart rate, arterial hematocrit, or arterial plasma protein concentration altered. These data indicate that the liver plays an important role in mediating the renal hyperemia and hyperfiltration observed following a physiologic infusion of glucagon.
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