NO Synthase Inhibition Increases Aldosterone in Humans

作者: James A.S. Muldowney , Stephen N. Davis , Douglas E. Vaughan , Nancy J. Brown

DOI: 10.1161/01.HYP.0000143852.48258.F1

关键词:

摘要: To test the hypothesis that NO influences aldosterone production in humans, we examined effect of N(G)-nitro-L-arginine methyl ester (L-NAME) on concentrations presence and absence precursor L-arginine (3 g TID) angiotensin-converting enzyme inhibitor ramipril (10 mg QD). Ten normal subjects were given L-NAME (66 microg/kg per min for 30 minutes) or vehicle random order separate days during placebo after randomized, double-blind treatment with L-arginine, ramipril, plus ramipril. Infusion significantly increased systolic blood pressure (all P<0.05) decreased heart rate P< =0.02) all 4 arms. After pretreatment, serum was higher infusion than (6.6+/-1.7 versus 3.3+/-0.5 ng/dL; P=0.045). Combined abolished this effect. There no plasma renin activity (PRA; P=0.297) angiotensin II (P=0.537). However, there a significant interactive time potassium (P=0.039). linear relationship between PRA concentration ([aldosterone]=3.9.PRA+1.9; r2=0.476; P=0.027) ([aldosterone]=7.2.PRA+3.1; r2=0.457; P=0.032), intercepts these lines different (P=0.029). ([aldosterone]=8.2 . [potassium]-28.9; r2=0.609; P=0.008) but not (P=0.313). These data suggest endogenous modulates synthesis humans.

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