AJP - Heart and Circulatory Physiology, Vol 246, Issue 1 104-H113, Copyright © 1984 by American Physiological Society
Vascular effects of arginine vasopressin, angiotensin II, and norepinephrine in adrenal insufficiency
S. Ishikawa and R. W. Schrier
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.
