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  • Title: Relationship between aldosterone and bradykinin.
    Author: Mersey JH, Williams GH, Hollenberg NK, Dluhy RG.
    Journal: Circ Res; 1977 May; 40(5 Suppl 1):I84-8. PubMed ID: 870233.
    Abstract:
    To assess relationships between plasma bradykinin and the individual elements of the renin-angiotensin-aldosterone system 11 normal subjects and five subjects with adrenal insufficiency were studied on an intake of 200 mEq sodium/100 mEq potassium. In adrenal insufficiency subjects, plasma bradykinin did not change when angiotensin II levels were increased by an infusion rate of 3 ng/kg per min for 30 minutes; plasma aldosterone remained undetectabel. In normal subjects, angiotensin II at 3 ng/kg per min or potassium at 20 mEq/hour infused intravenously for 2 hours both significantly increased plasma aldosterone levels, yet neither stimulus altered plasma bradykinin. Thus, acute elevations in angiotensin II and plasma aldosterone were not associated with changes in the levels of plasma bradykinin. In five additional normal subjects on an intake of 10 mEq sodium/100 mEq potassium, a threshold dose of converting enzyme inhibitor (SQ 20881) at 30 microng/kg was given intravenously. Five minutes after administration of the drug, blood pressure and plasma angiotensin II levels had significantly declined and plasma bradykinin levels had significantly increased (P is less than 0.02). Within 10-20 minutes, however, all had returned to control accompanied by a sustained increase in plasma renin activity, and a decrement in plasma aldosterone. Plasma renin activity, which had increased by more than 2-fold after the administration of the converting enzyme inhibitor, remained elevated until the completion of the study at 320 minutes. Eighty minutes after beginning the infusion, plasma aldosterone levels returned to control. Thus, the results suggest that plasma bradykinin correlates more closely with acute changes in plasma renin activity (and angiotensin I) than plasma aldosterone or angiotensin II, suggesting a role for converting enzyme in the regulation of both plasma renin activity and plasma bradykinin. Furthermore, the declines in blood pressure observed with converting enzyme inhibition may be attributable to both changes in plasma angiotensin II and plasma bradykinin concentrations. However, it is emphasized that these short-term studies may not reflect the role of bradykinin in the long-term control of blood pressure.
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