Nitric oxide: a potential mediator of amino acid-induced renal hyperemia and hyperfiltration.

作者: Julia R. Neuringer , Julia L. Troy , Barry M. Brenner , Sharon Anderson , Andrew J. King

DOI: 10.1681/ASN.V1121271

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摘要: The role of nitric oxide in the modulation systemic and renal hemodynamics was examined by using N omega-monomethyl-L-arginine (L-NMMA, 110 micrograms/kg/min), a competitive inhibitor conversion L-arginine to oxide. L-NMMA or saline vehicle (9.6 microL/min) infused intravenously into anesthetized euvolemic Munich-Wistar rats. After 30 min, resulted uniform increase mean arterial blood pressure (111 +/- 1 128 2 mmHg; P less than 0.05) modest reduction plasma flow rate (4.4 0.2 4.2 0.1 mL/min; 0.05), without change glomerular filtration (1.16 0.03 1.15 mL/min); had no effect on these parameters. These rats were then subdivided receive an intravenous infusion (37 either 10% glycine, 11.4% mixed amino acids, equiosmolar dextrose. pretreatment markedly attenuated glycine-induced hyperfiltration (10 6 versus 33 5%, vehicle; obliterated hyperemic response (-7 16 4%, 0.05). also caused blunting acid-induced (18 4 = 0.056) but failed curtail hyperemia (16 20 4%). Dextrose flow.(ABSTRACT TRUNCATED AT 250 WORDS)

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