Nitric oxide

A potential mediator of amino acid-induced renal hyperemia and hyperfiltration

Andrew J. King, Julia L. Troy, Sharon Anderson, Julia R. Neuringer, Mark Gunning, Barry M. Brenner

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

The role of nitric oxide in the modulation of systemic and renal hemodynamics was examined by using Nω-monomethyl-L-arginine (L-NMMA, 110 μg/kg/min), a competitive inhibitor of the conversion of L-arginine to nitric oxide. L-NMMA or saline vehicle (9.6 μL/min) was infused intravenously into anesthetized euvolemic Munich-Wistar rats. After 30 min, L-NMMA resulted in a uniform increase in mean arterial blood pressure (111 ± 1 to 128 ± 2 mm Hg; P<0.05) and a modest reduction in renal plasma flow rate (4.4 ± 0.2 to 4.2 ±0.1 mL/min; P<0.05), without change in glomerular filtration rate (1.16 ± 0.03 to 1.15 ± 0.03 mL/min); vehicle had no effect on these renal parameters. These rats were then subdivided to receive an intravenous infusion (37 μL/min) of either 10% glycine, 11.4% mixed amino acids, or equiosmolar dextrose. L-NMMA pretreatment markedly attenuated glycine-induced hyperfiltration (10 ± 6 versus 33 ± 5%, L-NMMA versus vehicle; P<0.05) and obliterated the renal hyperemic response (-7 ± 6 versus 16 ± 4%, L-NMMA versus vehicle; P <0.05). L-NMMA also caused modest blunting of the mixed amino acid-induced hyperfiltration (18 ± 4 versus 30 ± 4%, L-NMMA versus vehicle; P = 0.056) but failed to curtail the renal hyperemia (16 ± 6 versus 20 ± 4%). Dextrose had no effect on glomerular filtration rate or renal plasma flow. These results with mixed amino acids differed from those with glycine alone, presumably because the former was rich in L-arginine, the metabolic precursor for nitric oxide. For glycine-treated rats, urinary 3′,5′-cGMP excretion rates increased significantly in both vehicle- and L-NMMA-treated rats (6.1 ± 1.1 to 15.7 ± 2.4 and 7.9 ± 0.6 to 14.6 ± 0.6 pmol/min, respectively). In summary, nitric oxide appears to influence basal systemic, and to a lesser extent, basal renal vascular tone. Furthermore, the renal effects of mixed amino acids and glycine are, at least in part, sensitive to L-NMMA, suggesting that nitric oxide formation contributes to the renal vasodilation and hyperfiltration responses to acute amino acid infusion.

Original languageEnglish (US)
Pages (from-to)1271-1277
Number of pages7
JournalJournal of the American Society of Nephrology
Volume1
Issue number12
StatePublished - 1991
Externally publishedYes

Fingerprint

omega-N-Methylarginine
Hyperemia
Nitric Oxide
Kidney
Amino Acids
Glycine
Renal Plasma Flow
Arginine
Glomerular Filtration Rate
Arterial Pressure
Glucose
Intravenous Infusions
Vasodilation
Blood Vessels
Wistar Rats
Hemodynamics

Keywords

  • EDRF
  • Glycine
  • Hemodynamics
  • Kidney
  • N-monomethyl-L-arginine

ASJC Scopus subject areas

  • Nephrology

Cite this

King, A. J., Troy, J. L., Anderson, S., Neuringer, J. R., Gunning, M., & Brenner, B. M. (1991). Nitric oxide: A potential mediator of amino acid-induced renal hyperemia and hyperfiltration. Journal of the American Society of Nephrology, 1(12), 1271-1277.

Nitric oxide : A potential mediator of amino acid-induced renal hyperemia and hyperfiltration. / King, Andrew J.; Troy, Julia L.; Anderson, Sharon; Neuringer, Julia R.; Gunning, Mark; Brenner, Barry M.

In: Journal of the American Society of Nephrology, Vol. 1, No. 12, 1991, p. 1271-1277.

Research output: Contribution to journalArticle

King, AJ, Troy, JL, Anderson, S, Neuringer, JR, Gunning, M & Brenner, BM 1991, 'Nitric oxide: A potential mediator of amino acid-induced renal hyperemia and hyperfiltration', Journal of the American Society of Nephrology, vol. 1, no. 12, pp. 1271-1277.
King, Andrew J. ; Troy, Julia L. ; Anderson, Sharon ; Neuringer, Julia R. ; Gunning, Mark ; Brenner, Barry M. / Nitric oxide : A potential mediator of amino acid-induced renal hyperemia and hyperfiltration. In: Journal of the American Society of Nephrology. 1991 ; Vol. 1, No. 12. pp. 1271-1277.
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AU - Brenner, Barry M.

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N2 - The role of nitric oxide in the modulation of systemic and renal hemodynamics was examined by using Nω-monomethyl-L-arginine (L-NMMA, 110 μg/kg/min), a competitive inhibitor of the conversion of L-arginine to nitric oxide. L-NMMA or saline vehicle (9.6 μL/min) was infused intravenously into anesthetized euvolemic Munich-Wistar rats. After 30 min, L-NMMA resulted in a uniform increase in mean arterial blood pressure (111 ± 1 to 128 ± 2 mm Hg; P<0.05) and a modest reduction in renal plasma flow rate (4.4 ± 0.2 to 4.2 ±0.1 mL/min; P<0.05), without change in glomerular filtration rate (1.16 ± 0.03 to 1.15 ± 0.03 mL/min); vehicle had no effect on these renal parameters. These rats were then subdivided to receive an intravenous infusion (37 μL/min) of either 10% glycine, 11.4% mixed amino acids, or equiosmolar dextrose. L-NMMA pretreatment markedly attenuated glycine-induced hyperfiltration (10 ± 6 versus 33 ± 5%, L-NMMA versus vehicle; P<0.05) and obliterated the renal hyperemic response (-7 ± 6 versus 16 ± 4%, L-NMMA versus vehicle; P <0.05). L-NMMA also caused modest blunting of the mixed amino acid-induced hyperfiltration (18 ± 4 versus 30 ± 4%, L-NMMA versus vehicle; P = 0.056) but failed to curtail the renal hyperemia (16 ± 6 versus 20 ± 4%). Dextrose had no effect on glomerular filtration rate or renal plasma flow. These results with mixed amino acids differed from those with glycine alone, presumably because the former was rich in L-arginine, the metabolic precursor for nitric oxide. For glycine-treated rats, urinary 3′,5′-cGMP excretion rates increased significantly in both vehicle- and L-NMMA-treated rats (6.1 ± 1.1 to 15.7 ± 2.4 and 7.9 ± 0.6 to 14.6 ± 0.6 pmol/min, respectively). In summary, nitric oxide appears to influence basal systemic, and to a lesser extent, basal renal vascular tone. Furthermore, the renal effects of mixed amino acids and glycine are, at least in part, sensitive to L-NMMA, suggesting that nitric oxide formation contributes to the renal vasodilation and hyperfiltration responses to acute amino acid infusion.

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