The influence of the pituitary gland on sodium conservation, and plasma renin and renin substrate concentrations in the rat.

The responses of plasma renin and renin substrate concentrations to changes in dietary sodium intake have been investigated in normal and hypophysectomized rats. In the normal rat sodium deprivation for 13 days produced a striking increase in plasma renin concentration. However, unlike the response observed in other species, administration of 0.45 and 0.9 % sodium chloride in the drinking water failed to suppress the level of plasma renin below that observed in rats drinking 0.18% saline. No significant changes in plasma renin substrate concentration were induced by the various alterations in sodium intake. The changes observed in plasma renin concentration support the view that the renin-angiotensin system is involved in sodium conservation in the rat, perhaps in part via the stimulation of aldosterone secretion. In the hypophysectomized groups of animals similar changes in plasma renin concentration were observed in relation to changes in salt balance, indicating that the basic responsiveness of the system had not been modified. However, renin levels were slightly lower throughout in hypophysectomized animals but the differences were not significant. Hypophysectomy resulted in a significant fall in plasma renin substrate concentration. Other things being equal, the large fall in substrate concentration could be a major factor in reducing the circulating concentration of angiotensin II in vivo, and it might therefore be involved in the reduced aldosterone secretion described in sodium-depleted hypophysectomized animals. Whatever the effect of the pituitary upon, these interactions, the study indicates basically normal capacities for the hypophysectomized rat both to secrete renin and to conserve sodium under extremely rigorous conditions of stress. {Endocrinology 86: 824, 1970) T ROLE of the pituitary gland in the control of sodium metabolism and in the regulation of the renin-angiotensinaldosterone system is uncertain. Over 25 years ago, Swann (1) suggested that the pituitary exerted only slight influence upon the ability of the adrenal cortex to secrete sodium-retaining hormones. More recently, however, it has been shown that, in the absence of the pituitary, aldosterone secretion may fall considerably (2-10) and respond less readily to stimuli which normally cause increased release of the hormone (2, 6, 9, 10). Available data on the effect of pituitary hormones in restoring aldosterone secretion after hypophysectomy have been conflicting (2, 3, 11). In Received June 2,1969. Requests for reprints should be sent to: Dr. J. H. Laragh, 630 West 168th St. New York, N. Y. 10032. Supported by Grants HE-01275 and HE-05741 from the NIH, USPHS. 1 This work was performed during the tenure of a Lilly International Fellowship. the rat, the pituitary gland appears essential for the stimulation of aldosterone secretion which normally follows sodium deprivation (3, 8-10). Hypophysectomy caused a fall in aldosterone secretion even when the animals received a normal dietary intake of sodium and abolished or blunted the rise in secretion which would otherwise normally occur in intact rats during sodium depletion. Furthermore, this loss of response in hypophysectomized rats to sodium deprivation could be partially restored by injections of whole pitu-