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

Vascular effects of arginine vasopressin, angiotensin II, and norepinephrine in adrenal... MAP greater (P c 0.05) than that observed in glucocorticoiddeficient rats (107.7-84.8 mmHg, P < 0.02). In addition, the AVP antagonist causeda greater and more prolongedreduction in MAP in mineralocorticoid-deficient rats after the administration of either the angiotensin II antagonist or a-blocker. These results indicate that AVP, norepinephrine, and angiotensin II are involved in maintaining blood pressurein the mineralocorticoid-deficient state. 20-yr quest Manning and Sawyer have accomplished their goal of synthesizing an inhibitor to the hydrosmotic effect of AVP (27, 28, 31). This inhibitor blocks the antidiuretic effect of AVP without alteration in glomerular filtration or lute excretion rate (17); it has al been shown to inhibit [3H]AVP binding to papillary plasma membranes and to block the effect of AVP to stimulate adenylate cyclase in papillary collecting ducts (21) M’anning and Sawyer (23, 29, 30) have al developed inhibitors to the vascular effect of AVP. These inhibitors have shown that endogenous AVP may exert an important effect on circulatory homeostasis (1, il). On the other hand, the infusion of large amounts of vapressin in normal humans has not been found to be presr (14, 34). This may, however, be due to the more effective baroreceptor responses in humans http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

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

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Publisher
The American Physiological Society
Copyright
Copyright © 1984 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
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Abstract

MAP greater (P c 0.05) than that observed in glucocorticoiddeficient rats (107.7-84.8 mmHg, P < 0.02). In addition, the AVP antagonist causeda greater and more prolongedreduction in MAP in mineralocorticoid-deficient rats after the administration of either the angiotensin II antagonist or a-blocker. These results indicate that AVP, norepinephrine, and angiotensin II are involved in maintaining blood pressurein the mineralocorticoid-deficient state. 20-yr quest Manning and Sawyer have accomplished their goal of synthesizing an inhibitor to the hydrosmotic effect of AVP (27, 28, 31). This inhibitor blocks the antidiuretic effect of AVP without alteration in glomerular filtration or lute excretion rate (17); it has al been shown to inhibit [3H]AVP binding to papillary plasma membranes and to block the effect of AVP to stimulate adenylate cyclase in papillary collecting ducts (21) M’anning and Sawyer (23, 29, 30) have al developed inhibitors to the vascular effect of AVP. These inhibitors have shown that endogenous AVP may exert an important effect on circulatory homeostasis (1, il). On the other hand, the infusion of large amounts of vapressin in normal humans has not been found to be presr (14, 34). This may, however, be due to the more effective baroreceptor responses in humans

Journal

AJP - Heart and Circulatory Physiology – The American Physiological Society

Published: Jan 1, 1984

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