Faculty Collaboration Database

Inhibition of renal vascular 20-HETE production impairs autoregulation of renal blood flow. Am J Physiol 1994 Feb;266(2 Pt 2):F275-82

Date

02/01/1994

Pubmed ID

8141328

DOI

10.1152/ajprenal.1994.266.2.F275

Scopus ID

2-s2.0-0028296987 (requires institutional sign-in at Scopus site)   189 Citations

Abstract

The present study evaluated the role of endogenous P-450 metabolites of arachidonic acid (AA) on autoregulation of renal blood flow in rats. Whole kidney and cortical blood flows were well autoregulated when renal perfusion pressure was varied from 150 to 100 mmHg. Infusion of 17-octadecynoic acid (17-ODYA) into the renal artery (33 nmol/min) increased cortical and papillary blood flows by 12.6 +/- 2.5 and 26.5 +/- 4.6%, respectively. After 17-ODYA, autoregulation of whole kidney and cortical blood flows was impaired. Intrarenal infusion of miconazole (8 nmol/min) had no effect on autoregulation of whole kidney, cortical, or papillary blood flows. 17-ODYA (1 microM) inhibited the formation of 20-hydroxyeicosatetraenoic acid (20-HETE) and 11,12- and 14,15-epoxyeicosatrienoic acids (EETs) by renal preglomerular microvessels in vitro by 83.7 +/- 7.4% and 89.0 +/- 4.9%, respectively. Miconazole (1 microM) reduced the formation of EETs by 86.4 +/- 5.7%, but it had no effect on the production of 20-HETE. These results suggest that endogenous P-450 metabolites of AA, particularly 20-HETE, may participate in the autoregulation of renal blood flow.

Author List

Zou AP, Imig JD, Kaldunski M, Ortiz de Montellano PR, Sui Z, Roman RJ

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

Animals
Arachidonic Acid
Cytochrome P-450 Enzyme System
Fatty Acids, Unsaturated
Homeostasis
Hydroxyeicosatetraenoic Acids
In Vitro Techniques
Kidney
Kidney Cortex
Kidney Medulla
Kinetics
Male
Miconazole
Microcirculation
Muscle, Smooth, Vascular
Rats
Rats, Sprague-Dawley
Regional Blood Flow
Renal Circulation