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Ming Li, Tafline Fraser, Jian Wang* and Judith A Whitworth
Author(s) -
Whitworth Judith
Publication year - 1997
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.1440-1681.1997.tb02121.x
Subject(s) - dexamethasone , nitrite , endocrinology , medicine , arginine , blood pressure , glucocorticoid , adrenocorticotropic hormone , chemistry , nitrate , hormone , biochemistry , amino acid , organic chemistry
SUMMARY 1. The effects of L‐arginine treatment on dexamethasone‐induced hypertension were examined in the Sprague‐Dawley rat Seventy rats were randomly divided into the following eight groups: sham, dexamethasone (5 and 10 fig/day), L‐arginine (100 and 500 mg/kg per day), L‐arginine (100 or 500 mg/kg per day) + dexamethasone (10 ug/day), L‐arginine (520‐797 mg/kg per day in food) + dexamethasone (5 fig/day). Systolic blood pressure (SBP), bodyweight and plasma nitrate/nitrite concentration were measured. 2. Dexamethasone (5 and 10 ug/day) increased SBP in both sham and L‐arginine‐treated rats. Dexamethasone at 10 ug/day decreased bodyweight, but did not alter plasma nitrate/nitrite concentrations. 3. L‐Arginine (500 mg/kg per day, i.p.) increased plasma nitrate/nitrite concentrations in 10 ug/day dexamethasone‐treated rats. L‐Arginine did not alter blood pressure in either sham or dexamethasone‐treated rats. 4. Dexamethasone‐induced hypertension differs from adrenocorticotropic hormone (ACTH)‐induced hypertension in the rat in that it is not modified by L‐arginine. Thus, ACTH‐induced hypertension cannot be explained simply in terms of glucocorticoid activity.