Time Course of Enhanced Adrenal Responsiveness to Angiotensin on a Low Salt Diet.
Rogacz, Suzanne; Williams, Gordon H.; Hollenberg, Norman K.
15(4):376-380, April 1990.
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To assess the rate of activation of the renin-angiotensin-aldosterone axis and enhancement of adrenal responsiveness to angiotensin II (Ang II) with restriction of sodium intake, 16 healthy male subjects were placed initially on a 200 meq daily sodium intake; adrenal responsiveness to Ang II was assessed, and then daily sodium intake was reduced abruptly to 10 meq. Adrenal responses to Ang II were assessed again during the non-steady state interval 24 and 48 hours later, and after balance was achieved in 5-7 days. Renin-angiotensin system activation was evident within 24 hours after sodium intake was restricted. The increase in basal plasma aldosterone concentration and enhancement of the adrenal response to Ang II, on the other hand, tended to lag. Within 24 hours of restricting sodium intake, despite a significant increase in both plasma renin activity (1.0 /-0.2 vs. 2.4 /-0.7 ng/ml/hr, p < 0.01) and Ang II concentration (22.0 /-1.9 vs. 29.5 /-1.3 pg/ml, p < 0.05), there was no increase in basal plasma aldosterone concentration (10.4 /-1.3 vs. 11.7 /-1.2 ng/dl). At 48 hours, despite little further change in plasma renin activity or plasma Ang II concentration, there was a sharp increase in basal plasma aldosterone concentration (22.5 /-3.6 ng/dl, p < 0.01). The adrenal response to Ang II was increased significantly at 24 hours, evident at only a 10 ng/kg/min dose, but showed progressive further enhancement with time. Early enhancement was not related to shifts in potassium balance as none occurred, but later progressive enhancement could reflect in part negative potassium balance, as a small but consistent element of negative balance occurred. These observations add further support to the concept that some unidentified factor other than plasma Ang II concentration or potassium balance, but related to sodium balance, modifies the adrenal response to Ang II. Available evidence suggests that enhancement reflects events at the terminal step of aldosterone biosynthesis.
(C) 1990 American Heart Association, Inc.