The effect of estrogens on renal sodium excretion in the dog.

Abstract

The effects of estrogens on electrolyte balances were studied in dogs. In doses of 1 mg or 250 mug/day, 17 beta-estradiol produced moderate sodium retention, whereas 100 mug/day produced only slight sodium retention. Estriol produced about the same degree of sodium retention as did estradiol. The administration of estradiol during the injection of large doses of DOCA produced the same degree of sodium retention as estradiol administered alone. Also, the injection of DOCA to estrogen-treated dogs resulted in a transitory sodium retention, followed by a sodium escape and a return to the previous balance level. Estradiol given to dogs with an arteriovenous shunt that had failed previously to show sodium escape during treatment with DOCA produced the same degree of sodium retention as that observed during estradiol administration to normal dogs. Five adrenalectomized dogs maintained on cortisone and DOCA had normal sodium balances during the control period but showed a retention of sodium during the administration of estradiol; administration. Four adrenalectomized dogs maintained only on cortisone were in negative sodium balance during the control period, but during estradiol treatment they showed a retention of sodium. These studies provide evidence that estrogens promote sodium retention in dogs by mechanisms other than by decreasing the glomerular filtration rate, increasing the secretion rates of adrenal steroids, or affecting the sodium escape mechanism. It is suggested that estrogens might act directly on the renal tubules at receptors other than those for the adrenal mineralocorticoids to produce sodium retention.