Reciprocal Variations in Urinary Cortisol and Aldosterone in Response to Increased Salt Intake in Humans

Abstract

In this study utilizing isotopic techniques for measuring specific corticoids, the oral administration of 8-16 g of NaCl daily for 6-10 days in addition to a constant dietary intake resulted in an increased rate of urinary cortisol excretion in each of 6 subjects. There were rises in the cortisol secretion rates measured in 2 of the subjects, although these were proportionately less than the corresponding increases in cortisol excretion. Although these results seemingly conflict with earlier reports that cortisol production is unresponsive to changes in salt balance, the apparent contradiction is explained by the inability to detect subtle fluctuations with the corticoid measurements previously employed, whereas the methods utilized in this study afford much greater sensitivity. The anticipated lowering of the aldosterone excretion rate occurred as a result of the increased salt intake and the pattern of the aldosterone response was virtually the reciprocal of that of cortisol. Urinary corticosterone, pregnanediol and pregnanetriol were also measured by isotope derivative techniques, but there were only slight or suggestive increases associated with the cortisol responses in a few instances. It is possible that the cortisol responses observed here could reflect a physiologically active, ACTH dependent salt-dissipating mechanism. Although no adrenocortical hormone with direct salt-losing action has yet been identified, there is evidence that cortisol and several corticoids and precursors in their biosynthesis can inhibit the Na retaining activity of aldosterone. However, the presumed increases in cortisol produc-tion in this study were modest, so that it is problematic whether the associated increments in these inhibitory steroids would be sufficient to have significant natriuretic effects. On the other hand, such cortisol responses to excessive salt, if prolonged, would be of sufficient magni-tude to impose some physiologic effects, so that even if unrelated to a salt-dissipating function, they might result in clinical consequences.