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Effects of chronic nitric oxide synthase (NOS) inhibition on renal blood flow
Author(s) -
McAllister Richard Murray,
Johnson Robert L,
Newcomer Sean C,
Laughlin Maurice Harold
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a498
Subject(s) - renal blood flow , bradykinin , nitric oxide synthase , sodium nitroprusside , endocrinology , nitric oxide , medicine , vasomotor , chemistry , blood flow , kidney , renal circulation , endothelium , blood pressure , receptor
This study tested the hypothesis that nitric oxide contributes to control of renal blood flow. To test this hypothesis, control swine drank tap water (Con; n=23) while treated swine drank water with the NOS inhibitor NG‐nitro‐L‐arginine methyl ester (L‐N, 7.6±0.5 mg/kg/d over ≥ 1 mo; n=19). Treatment efficacy was evidenced by increased blood pressure (Con, 84±4 mmHg; L‐N, 118±7; P<0.05) and decreased plasma NOx (Con, 12.2±1.9 μM; L‐N, 6.8±0.7; P<0.05). Tissue blood flows were measured using radiolabelled microspheres. At rest, renal blood flow was lower with chronic NOS inhibition (Con, 317±18 ml/min/100 g; L‐N, 235±14; P<0.05), but during exercise (8 km/h running) renal blood flow did not differ between groups. Renal arterial segments were isolated and vasomotor responses determined in vitro. Endothelium‐dependent relaxation responses to bradykinin (BK) were reduced (P<0.05) with chronic NOS inhibition (at 1.0 μM BK: Con, 97±1%; L‐N, 86±4). Endothelium‐independent relaxation to sodium nitroprusside did not differ between groups. These data indicate that chronic NOS inhibition decreases resting renal blood flow. Further, if changes observed in the renal artery also occur in resistance vessels, our data suggest that the endothelium participates in control of renal blood flow. Supported by NIH RR18276.