AJP - Renal Physiology, Vol 260, Issue 6 787-F792, Copyright © 1991 by American Physiological Society

ARTICLES

Hormonal mediators of amino acid-induced glomerular hyperfiltration in humans

L. Wada, B. R. Don and M. Schambelan
Medical Service, San Francisco General Hospital Medical Center, California 94110.

It has been speculated that glucoregulatory hormones and/or renal autacoids mediate the increase in glomerular filtration rate (GFR) induced by the administration of protein or amino acids. Because infusion of a mixture of amino acids (AA mix), but not of branched-chain amino acids (BCAA) alone, increases GFR, we performed a crossover study in seven normal subjects in which the glomerular hemodynamic effects of separate 3-h infusions of these two amino acid solutions were compared with changes in potential mediators of this response, i.e., glucoregulatory hormones, renin, vasodilatory prostaglandins (PGs), and guanosine 3',5'-cyclic monophosphate (cGMP). As expected, infusion of the AA mix but not BCAA resulted in a prompt and sustained increase in GFR. Both infusions caused a significant increase in plasma insulin, whereas glucagon increased only with the AA mix. Plasma growth hormone was initially unchanged with both infusions but increased after 2 h of BCAA. Neither infusion significantly increased the urinary excretion of PGE2, 6-keto-PGF1 alpha, or cGMP. Both infusions resulted in a small but significant decrease in plasma renin activity. Infusion of BCAA but not the AA mix resulted in a progressive decrease in plasma glucose and potassium concentrations and an increase in renal sodium reabsorption that may have resulted from stimulation of insulin secretion that was not counterbalanced by a simultaneous increase in glucagon. Thus only changes in glucagon exhibited a significant temporal relationship with changes in GFR, lending further support to a role for glucagon as a mediator of amino acid-induced glomerular hyperfiltration.

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