Glucagon inhibits urinary acidification in the rat.

Abstract

The effects on urinary acidification of an acute infusion of glucagon (GLU) were studied by paired experiments in plasma-replete rats whose endogenous GLU secretion was restrained by a 0.7 ng.min-1.g body wt-1 somatostatin infusion. GLU did not affect the glomerular filtration rate in any of the plasma-replete rats studied. In 10 thyroparathyroidectomized (TPTX) rats and five intact rats subjected to hypotonic volume expansion, a low-dose (0.02 ng.min-1.g body wt-1) GLU infusion that raised the plasma GLU concentration from 302 +/- 63 to 1,010 +/- 140 pg/ml significantly increased the urinary bicarbonate excretion and decreased the urinary net acid excretion; a high-dose (0.05 ng.min-1.g body wt-1) glucagon infusion in the intact rats, that increased the plasma GLU concentration to 1,609 +/- 307 pg/ml, further enhanced the urinary bicarbonate excretion rate. In intact plasma-replete rats that were not subjected to a hypotonic volume expansion, low- and high-dose GLU infusions failed to affect the urinary bicarbonate excretion rate. Finally, no change in urinary excretion rates was noted in TPTX volume-expanded time control rats. We conclude that 1) physiological increments in plasma GLU concentration decrease urinary acidification by affecting the tubular H+/bicarbonate transport; 2) the bicarbonaturic effect of GLU may be blunted by the renal effects of high circulating antidiuretic hormone levels, or may be facilitated in an undetermined manner by hypotonic volume expansion.