Relative roles of nitric oxide, prostanoids and angiotensin II in the regulation of canine glomerular hemodynamics. A micropuncture study.

摘要: Glomerular hemodynamics are controlled by a variety of physical, nervous and hormonal factors including the potent vasoconstrictors, angiotensin (ANG) II endothelin-1 (ET-1), vasodilator prostanoids (prostaglandin = PG) nitric oxide (NO). Since no micropuncture data on canine kidney exist with respect to relative roles endogenous vasoactive hormones/autacoids NO, PG ANG in modulating glomerular hemodynamics, present study using technique anesthetized dogs normal salt intake, we investigated effects these means L-arginine analog, N(omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME), competitive NO synthase (NOS) inhibitor, cyclooxygenase inhibitor indomethacin (INDO), AT(1) receptor blocker EXP 3174. An intrarenal arterial (i.r.a.) bolus (within 5 min) 2.5 mg L-NAME led significant decrease total renal blood flow (RBF) single nephron (SNGBF) from 4.46 +/- 0.51 3.52 0.41 ml/min/g weight 0.393 0.041 0.341 0.037 microl/min (p < 0.01), respectively, without change filtration rate (GFR). The increase arteriolar resistance was more pronounced at efferent (+31%) than afferent (+13%) arteriole, K(f) decreased 4.5 0.5 3.7 0.4 nl/min/mm Hg 0.01). INDO (5 mg/kg i.v. followed 0.17 mg/kg/min i.v.) had effect hemodynamics. 3174 (30 microg/kg/min i.r.a.) increased RBF SNGBF 4.35 0.45 4.99 0.50 0.403 0.028 0.478 0.039 an GFR. It reduced 25% as compared 13% level. 5.1 8.1 0.6 mm 0.01) presence effective pressure 13.2 1.7 8.3 1.0 hemodynamic were unaltered pretreatment or 3174, whereas its tubular restored Thus, first dog sodium intake conclude that (1) acute inhibition NOS decreases due vasoconstriction and, pronounced, arterioles. simultaneously K(f), GFR remains unaltered. (2) These not mediated II. tonic activity plays important role maintaining kidney.