Effect of angiotensin ii on the renal response to amino acid in rats

Abstract

Administration of the nitric oxide (NO) synthase blocker, NG-monomethyl L-arginine prevents the increase in glomerular filtration rate (GFR) normally observed with glycine, an effect that is restored by angiotensin II (All) blockers. These findings suggest that changes in NO and All dictate the presence or absence of renal vasodilation during amino acid (AA) infusion. We examined the effect of branched-chain (BCAA) and non-branched-chain (NBCAA) AA on GFR, NO, and All to determine if abnormal NO or All responses could explain the absence of vasodilation with BCAA. Our findings demonstrated that NBCAA increased GFR and NO and did not modify All, either plasma (Allp) or kidney (Allk) All. The response with BCAA was strikingly different. L-Valine increased GFR without modifying NO or All. L-Leucine increased Allk and NO but did not increase GFR. Administration of All blockers (captopril or losartan) was associated with an increase in GFR during infusion of leucine. Single nephron studies demonstrated that increased Allk with L-leucine was associated with decreased absolute proximal reabsorption and probably activation of the tubuloglomerular feedback. An AA-specific increase in Allk is critical to inhibition of the normal renal response to AA infusion. NO generation is an important mediator but not the sole mechanism that determines the increase in GFR during amino acid infusion.