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 blockade, stop-flow pressure (SFP; 48.2 +/- 2.0 vs. 58.9 +/- 2.3 mmHg, P less than 0.01), and proximally determined single-nephron glomerular filtration rate (SNGFR-TPC; 73.9 +/- 7.0 vs. 93.4 +/- 7.6 nl/min, P less than 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 less than 0.05), renal blood flow (RBF; 4.60 +/- 0.18 vs. 5.73 +/- 0.22 ml.min-1.g kidney wt-1, P less than 0.01), and glomerular filtration rate (GFR; 0.885 +/- 0.034 vs. 1.116 +/- 0.034 ml.min-1.g kidney wt-1, P less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)