Diabetes insipidus with renal resistance to vasopressin in the desoxycorticosterone-treated dog: a possible role for prostaglandins.
We examined the release of vasopressin and the renal response to exogenous vasopressin before and during desoxycorticosterone acetate (DOCA) administration in the dog. As treatment with DOCA produced potassium loss, urine volume increased, urinary osmolality decreased, and urinary PGE2 tended to increase. The increase in urine volume was accompanied by increases in serum sodium, in plasma osmolality and in plasma arginine vasopressin. The threshold for vasopressin release measured during polyuria was higher than control but the rate of vasopressin release was unchanged. The DOCA-induced polyuria was not affected by treatment with vasopressin which further increased plasma vasopressin. Treatment with indomethacin which corrected the increase in urinary PGE2 excretion but not the hypokalemia, restored the renal responsiveness to vasopressin, decreased the secretion of vasopressin, and corrected the polyuria and the hypernatremia. These findings suggest that DOCA-induced polyuria is attributable to a decrease in renal responsiveness to vasopressin which may be mediated in part by an increase in the renal synthesis of prostaglandins.
D000818:Animals; D001834:Body Water / Q000378:metabolism; D003900:Desoxycorticosterone; D003919:Diabetes Insipidus / Q000139:chemically induced* / Q000503:physiopathology / Q000652:urine; D015232:Dinoprostone; D004285:Dogs; D005260:Female; D011141:Polyuria / Q000139:chemically induced* / Q000503:physiopathology / Q000652:urine; D011188:Potassium / Q000097:blood; D011458:Prostaglandins E / Q000652:urine*; D014667:Vasopressins / Q000097:blood / Q000378:metabolism*
D011458:Prostaglandins E; D014667:Vasopressins; D003900:Desoxycorticosterone; D015232:Dinoprostone; D011188:Potassium