Renin-angiotensin system and cardiovascular homeostasis in adrenal insufficiency
Berns, A.S.; Pluss, R.G.; Erickson, A.L.; Anderson, R.J.; Mcdonald, K.M.; Schrier, R.W.
American Journal of Physiology 233(6): F509-F513
1977
ISSN/ISBN: 0002-9513 PMID: 596449 Document Number: 116022
The etiology and physiological significance of hyperreninemia in adrenal insufficiency were examined in conscious, adrenalectomized dogs. The animals were studied under conditions of full hormonal replacement (control), glucocorticoid deficiency and mineralocorticoid deficiency. Plasma renin activity was normal in the control dogs (2.3 .+-. 1.6 ng/ml per h) and slightly but not significantly elevated (5.2 .+-. 3.2 ng/ml per h) in the glucocorticoid-deficient animals. Mineralocorticoid deficiency was associated with significant elevations in plasma renin activity (27.2 .+-. 6.2 ng/ml per h). Infusion of [1-sarcosine, 8-glycine]angiotensin II was associated with hypotension in both glucocorticoid and mineralocorticoid deficiency. In mineralocorticoid deficiency blood pressure fell 28 mmHg (P < 0.001) and was associated with significant decreases in peripheral vascular resistance, stroke volume and glomerular filtration rate. In glucocorticoid deficiency angiotensin inhibition resulted in a 10 mmHg fall in blood pressure (P < 0.05) and was associated with significant decreases in cardiac output and stroke volume. Mineralocorticoid deficiency and the concomitant volume depletion are the primary stimuli to hyperreninemia in adrenocortical insufficiency. The renin-angiotensin system plays an important role in the maintenance of blood pressure and cardiovascular homeostasis in both glucocorticoid and mineralocorticoid deficiency.