SINGLE-NEPHRON RESPONSES TO SYSTEMIC ADMINISTRATION OF AMINO-ACIDS IN DOGS

It has been suggested that the tubuloglomerular feedback (TGF) system is responsible for renal vasodilation during systemic infusion of amino acid solutions. We evaluated the effect of intravenous administration of amino acids (serine, alanine, proline, and glycine; total dose of 0.075 mmol of amino acids.kg body wt-1.min-1) on whole kidney and single-nephron hemodynamics in pentobarbital sodium-anesthetized dogs. At spontaneous renal arterial pressure (RAP; 125.4 +/- 4.7 mmHg), measurements of single-nephron function obtained during tubular blockage, stop-flow pressure (SFP; 48.2 +/- 2.0 vs. 58.9 +/- 2.3 mmHg, P < 0.01), and proximally determined single-nephron glomerular filtration rate (SNGFR-TPC; 73.9 +/- 7.0 vs. 93.4 +/- 7.6 nl/min, P < 0.01) increased in parallel to the increases of outer cortical blood flow (OCBF; 15.4 +/- 1.1 vs. 19.1 +/- 1.5 units, P < 0.05), renal blood flow (RBF; 4.60 +/- 0.18 vs. 5.73 +/- 0.22 ml.min-1.g kidney wt-1, P < 0.01), and glomerular filtration rate (GFR; 0.885 +/- 0.034 vs. 1.116 +/- 0.034 ml.min-1.g kidney wt-1, P < 0.01). Free-flow tubular fluid-to-plasma inulin ratios, determined from late proximal recollections during saline (control) and amino acid infusions failed to provide evidence for altered proximal reabsorption rate (1.63 +/- 0.12 vs. 1.58 +/- 0.17 during amino acids, NS). At reduced RAP (92.6 +/- 1.9 mmHg), where it is presumed that TGF-mediated vasodilation is already near maximal, the vasodilatory response to amino acid infusion was intact and single-nephron parameters measured during tubular blockade increased to the same extent as OCBF, RBF, and GFR. The increases in SNGFR observed at reduced RAP were attributable to a reduction of afferent arteriolar resistance (R(a)) and enhancement of mean effective filtration pressure (P < 0.05), with no associated change in the glomerular ultrafiltration coefficient. During infusion of amino acids at 0.025, 0.075, or 0.225 mmol.kg-1.min-1, studies of RBF, GFR, and OCBF during stepwise reductions of RAP demonstrated that autoregulatory control of RBF, GFR, and OCBF were intact at the lowest amino acid infusion rate and only mildly impaired by the highest dose. These results are consistent with the hypothesis that a substantial component, if not all, of the renal vasodilation in response to amino acid infusion is independent of the TGF control mechanism.