Angiotensin and electrolyte excretion in renovascular hypertension
- 31 May 1965
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Legacy Content
- Vol. 208 (6) , 1087-1092
- https://doi.org/10.1152/ajplegacy.1965.208.6.1087
Abstract
Under conditions of saline, urea, ADH infusion diuresis during anesthesia we observed that in normal rats angiotensin infusion regularly produced natriuresis and diuresis, the degree of which was more closely related to dosage than to increment in blood pressure. Potassium excretion often did not rise appreciably or actually fell during natriuresis, suggesting inhibition of tubular secretion. In animals with a clamp on the left renal artery in which hypertension did not ensue, the renal response to angiotensin was strikingly changed when studied by bilateral ureteral catheterization. Instead of diuresis the peptide produced either no effect or sodium and water retention in both kidneys. In the hypertensive rats, angiotensin consistently produced marked diuresis on the clipped side. Sodium excretion increased much more than urine flow. Simultaneously, in the opposite, unprotected kidney, angiotensin produced quite different effects—sodium and water excretion either did not change or were reduced. Renovascular reflexes and renal renin activity may be involved in determining whether angiotensin induces sodium retention or natriuresis.Keywords
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