Faculty Collaboration Database

Kinin actions on renal papillary blood flow and sodium excretion. Hypertension 1993 Jun;21(6 Pt 2):961-5

Date

06/01/1993

Pubmed ID

8505107

DOI

10.1161/01.hyp.21.6.961

Scopus ID

2-s2.0-0027263226 (requires institutional sign-in at Scopus site)   87 Citations

Abstract

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.

Author List

Mattson DL, Cowley AW Jr

Author

Allen W. Cowley Jr PhD Professor in the Physiology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Arginine
Bradykinin
Captopril
Diuresis
Kidney Medulla
Male
NG-Nitroarginine Methyl Ester
Natriuresis
Rats
Rats, Inbred Strains
Renal Circulation
Sodium Chloride