Sensitivity to Angiotensin and Adrenocorticotrophic Hormone in the Sodium Deficient Rat

The effect of sodium deficiency, produced by 1 week of dietary salt restriction, on the adrenal response to angiotensin and adrenocorticotrophin (ACTH), singly and together, has been studied in acutely hypophysectomized-nephrectomized rats. Adrenal response was determined by the rate of secretion of aldosterone and corticosterone into adrenal vein blood as measured by the double isotope method. In sodium replete animals angiotensin did not significantly influence the secretion rate of either hormone. In sodium deficient animals it produced a significant increase in the secretion rate of aldosterone but not corticosterone. ACTH produced a significant increase in the secretion rates of both hormones. The response was similar in sodium replete and sodium deficient animals. When infused together in sodium replete animals the effect was no greater than with ACTH alone. However, when both hormones were infused together into sodium deficient animals the response in aldosterone secretion was even greater than the sum of the responses produced separately. Corticosterone secretion was no greater than it was with ACTH alone, regardless of previous diet. It is concluded that sodium deficiency in the rat sensitizes the aldosterone secreting mechanism to angiotensin but does not increase its sensitivity to ACTH. The synergistic effect on aldosterone secretion observed in the sodium deficient animals may be explained as a potentiation of the angiotensin effect by the increased availability of precursors when ACTH is infused at the same time. The present studies indicate that after 1 week of dietary salt restriction the adrenal cortex is sufficiently sensitive to angiotensin to allow for the demonstration of a significant effect on the secretion rate of aldosterone by the infusion of modest amounts of the hormone. The results support the view that angiotensin is involved in the adrenal response to sodium deficiency in the rat. (Endocrinology83: 1108, 1968)