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INHIBITION OF NO SYNTHESIS HAS AN ADDITIVE EFFECT ON HYPERTENSION INDUCED BY ACTH IN CONSCIOUS RATS
Author(s) -
Li Ming,
Dusting G. J.,
Whitworth Judith A.
Publication year - 1992
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.1440-1681.1992.tb00403.x
Subject(s) - medicine , endocrinology , blood pressure , nitric oxide , adrenocorticotropic hormone , urine , hemodynamics , chemistry , hormone
SUMMARY 1. The haemodynamic and metabolic effects of oral intake of ∼30 mg/kg per day N ‐nitro‐ l ‐arginine (NOLA) were examined in sham and adrenocorticotrophin (ACTH, 0.5 mg/kg per day) treated conscious Sprague‐Dawley rats ( n = 33). 2. NOLA administration produced an increase in systolic blood pressure of 24±6 mmHg ( P < 0.001), but did not alter food or water intake, urine volume or electrolyte excretion in rats not treated with ACTH. 3. Compared with sham injection, ACTH‐treated rats demonstrated an increase in systolic blood pressure (water + sham, 3±1 mmHg; water + ACTH, 16±3 mmHg; P < 0.001), loss of bodyweight, and increases in water intake and urine volume. 4. The magnitude of the blood pressure rise in ACTH‐treated rats was greater in those receiving NOLA than in those drinking water only (water + ACTH, 16±3 mmHg; NOLA + ACTH, 37±3 mmHg; P < 0.05). Metabolic changes were similar. 5. Inhibition of nitric oxide is unlikely to be a major determinant of ACTH‐induced hypertension in the rat, since NOLA increased blood pressure whether or not ACTH was administered, indicating an additive effect of ACTH and NOLA administration.