Hormonal mediators of amino acid-induced glomerular hyperfiltration in humans.

Abstract

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.