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THE NITRIC OXIDE SYSTEM AND CORTISOL‐INDUCED HYPERTENSION IN HUMANS
Author(s) -
Kelly John J,
Tam Sim H,
Williamson Paula M,
Lawson Jane,
Whitworth Judith A
Publication year - 1998
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1998.tb02349.x
Subject(s) - nitrite , nitrate , nitric oxide , medicine , endocrinology , arginine , chemistry , blood pressure , nitric oxide synthase , hydrocortisone , biochemistry , amino acid , organic chemistry
SUMMARY 1. The aim of the present study was to assess the role of the nitric oxide (NO) system in cortisol‐induced hypertension in humans. 2. Plasma and urinary nitrate/nitrite concentrations and plasma concentrations of arginine and symmetric (SDMA) and asymmetric (ADMA) dimethyl arginine were measured in six subjects on a restricted nitrate diet who were treated with 80 mg/day Cortisol and in subjects on an unrestricted nitrate diet who were treated with Cortisol (80 mg/day, n = 6, or 200 mg/day, n = 10) for 5 days. 3. Cortisol significantly increased systolic and mean arterial pressure. Significant reductions in plasma nitrate/nitrite concentrations were observed in subjects on a restricted nitrate diet on days 3, 4 and 5 of Cortisol treatment (to 11±1, 10±1, 11± pmol/L, respectively) compared with pretreatment (16±1 pmol/L; P<0.01) .There were no significant changes in plasma arginine, ADMA or SDMA concentrations. 4. Cortisol treatment significantly increased blood pressure and reduced plasma nitrate/nitrite concentrations. Reductions in plasma nitrate concentrations are not explained by changes in substrate availability or in endogenous nitric oxide synthase inhibitors. These data support a role for the NO system in cortisol‐induced hypertension in humans.