Hypertension, Vol 21, 961-965, Copyright © 1993 by American Heart Association
DL Mattson and AW Cowley Jr
Infusion of bradykinin into the renal medullary interstitium (0.1
micrograms/min, n = 6) significantly increased renal papillary blood flow
as measured by laser-Doppler flowmetry to 117 +/- 3% of control without
altering cortical blood flow or blood pressure in anesthetized
Munich-Wistar rats. In animals prepared for clearance studies, renal
medullary bradykinin infusion did not alter total renal blood flow,
glomerular filtration rate, or renal interstitial hydrostatic pressure but
increased urine flow by 100%, sodium excretion by 111%, and fractional
sodium excretion by 107%. No changes occurred in mean arterial pressure or
contralateral kidney function during the interstitial bradykinin infusion.
Blockade of endogenous kinin degradation by interstitial infusion of
captopril (1 mg/hr) significantly increased papillary blood flow by 21 +/-
5% without altering cortical blood flow. Pretreatment with the nitric oxide
inhibitor NG-nitro-L-arginine-methyl ester (2 micrograms/min, n = 7)
eliminated the increase in papillary blood flow associated with either
bradykinin or captopril infusion. We conclude that renal medullary
interstitial infusion of bradykinin increases sodium and water excretion,
which is associated with a selective increase in papillary blood flow by a
nitric oxide-dependent mechanism.
ARTICLES
Kinin actions on renal papillary blood flow and sodium excretion
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
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