Vascular effects of arginine vasopressin, angiotensin II, and norepinephrine in adrenal insufficiency.

Plasma arginine vasopressin (AVP) levels were 9.6 pg/ml in the mineralocorticoid-deficient rats, a value significantly greater than 4.8 pg/ml in the glucocorticoid-deficient rats (P less than 0.05), and 1.6 pg/ml in controls (P less than 0.001). The AVP antagonist of the vascular effect of AVP, [1(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine] AVP, [d(CH2)5Tyr(Me)AVP] (5 micrograms/kg), decreased mean arterial pressure (MAP) from 76.5 to 71.6 mmHg (P less than 0.01) in mineralocorticoid-deficient rats on day 10 but not in glucocorticoid deficient rats on day 14 (113.2-111.6 mmHg, NS) or in control rats (109.7-110.2 mmHg, NS). Plasma renin activity was 40.7 ng X ml-1 X h-1 in mineralocorticoid-deficient rats and 7.2 in glucocorticoid-deficient rats (P less than 0.001). The angiotensin II antagonist, [Sar1-Gly8]angiotensin II (5 micrograms X kg-1 X min-1), decreased MAP from 69.3 to 53.2 mmHg in mineralocorticoid-deficient rats (P less than 0.001) but not in glucocorticoid-deficient rats. Plasma norepinephrine was 1,138 pg/ml in mineralocorticoid-deficient rats and 251 pg/ml in glucocorticoid-deficient rats (P less than 0.001). The alpha-adrenergic blocker, phenoxybenzamine (3 mg/kg), reduced MAP from 82 to 51 mmHg in mineralocorticoid deficient rats (P less than 0.005), a decrease in MAP greater (P less than 0.05) than that observed in glucocorticoid-deficient rats (107.7-84.8 mmHg, P less than 0.02). In addition, the AVP antagonist caused a greater and more prolonged reduction in MAP in mineralocorticoid-deficient rats after the administration of either the angiotensin II antagonist or alpha-blocker. These results indicate that AVP, norepinephrine, and angiotensin II are involved in maintaining blood pressure in the mineralocorticoid-deficient state.