Endocrinology, Vol 133, 2469-2473, Copyright © 1993 by Endocrine Society

ARTICLES

Neither endogenous nor exogenous bradykinin stimulates aldosterone in vivo

VM Rudichenko, OA Carretero and WH Beierwaltes
Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Michigan 48202-2689.

It has been suggested that bradykinin (BK) can directly stimulate aldosterone secretion in vitro. Both chronic and acute studies were performed to determine whether we could show a pathway by which BK could stimulate plasma aldosterone in vivo. Chronic studies employed four groups of eight rats fed either a normal sodium or a sodium- restricted diet over 9 days. Half of the rats received infusion of a saline vehicle, and the others received the BK B-2 receptor antagonist HOE-140 at a rate of 200 micrograms/kg.day over 7 days via a sc implanted osmotic minipump. This rate was derived from studies showing that HOE-140 blocked pharmacological doses of exogenous BK. With a normal diet, there was no difference in plasma aldosterone in vehicle- treated rats vs. those treated with HOE-140 (368 +/- 55 vs. 329 +/- 66 pg/ml, respectively). Sodium restriction increased plasma aldosterone 10-fold, but again there was no difference between vehicle-treated rats and those treated with HOE-140 (2964 +/- 439 vs. 3755 +/- 475 pg/ml, respectively). Acute studies employed two groups of six rats. Direct suprarenal intraaortic infusion of 2 micrograms/min BK or saline vehicle was performed over 2 h. Plasma aldosterone was not changed in vehicle-treated groups, but decreased by 22% (P < 0.05) after BK infusion. Thus, blockade of kinin B-2 receptors had no effect on plasma aldosterone in normal or sodium-restricted diet rats. Acute BK infusion did not increase plasma aldosterone. We conclude that although BK may stimulate aldosterone in vitro, we found no physiological correlate to suggest that BK regulates plasma aldosterone in vivo.

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