Gullner H G, West D, Gill J R, Robertson G L
Hypertension-Endocrine Branch, National Heart, Lung, and Blood Institute, Bethesda, Md.
Ren Physiol. 1987;10(1):40-6. doi: 10.1159/000173112.
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.
我们研究了在给犬注射醋酸去氧皮质酮（DOCA）之前及期间，血管加压素的释放情况以及肾脏对外源性血管加压素的反应。由于DOCA治疗导致钾流失，尿量增加，尿渗透压降低，尿中前列腺素E2（PGE2）有增加趋势。尿量增加伴随着血清钠、血浆渗透压和血浆精氨酸血管加压素升高。多尿期间测得的血管加压素释放阈值高于对照组，但血管加压素释放速率未变。DOCA诱导的多尿不受血管加压素治疗影响，血管加压素治疗进一步增加了血浆血管加压素。吲哚美辛治疗纠正了尿中PGE2排泄增加，但未纠正低钾血症，恢复了肾脏对血管加压素的反应性，减少了血管加压素分泌，并纠正了多尿和高钠血症。这些发现表明，DOCA诱导的多尿归因于肾脏对血管加压素反应性降低，这可能部分由肾脏前列腺素合成增加介导。
