Bradykinin and renal function in normal man: effects of adrenergic blockade

¹ Clinical Endocrinology Branch and Experimental Therapeutics Branch, National Heart Institute, National Institutes of Health, Bethesda, Maryland

Renal function was studied in five normal subjects during the infusion of bradykinin at 0.1 and 0.4 µg/kg per min, and in four additional normal subjects during the infusion of norepinephrine at dosages beginning with 1–3 µg/ min. Bradykinin at both dosages decreased glomerular filtration rate (GFR) and tended to increase renal blood flow (ERPF). It increased sodium excretion (U_NaV) at the lower dosage, but did not increase it further at the higher dosage. At all dosages, norepinephrine decreased ERPF and U_NaV. The effects of bradykinin cannot be explained solely as effects of norepinephrine released by the bradykinin. During adrenergic blockade produced by guanethidine, bradykinin, 0.1 µg/kg per min, slightly decreased GFR and U_NaV; at 0.4 µg/kg per min, it further decreased GFR and U_NaV and tended to decrease ERPF as well. It did not lower blood pressure. The data suggest that in normal man, bradykinin increases U_NaV only at low dosages. During adrenergic blockade, endogenous release of angiotensin could have prevented bradykinin from lowering blood pressure and could have caused the decreases in GFR, ERPF, and U_NaV. A possible role is suggested for bradykinin in the physiologic control of renal function, and as a causative agent in producing the changes in renal function found in certain disease states characterized by excessive production of kinins.

Note:
With the Technical Assistance of Isabelle M. Ambrose and George W. Smith II

Key Words: glomerular filtration rate • renal plasma flow • sodium excretion • norepinephrine

Submitted on March 2, 1965