Effect of P-450 omega-hydroxylase metabolites of arachidonic acid on tubuloglomerular feedback. Am J Physiol 1994 Jun;266(6 Pt 2):F934-41
Date
06/01/1994Pubmed ID
8023972DOI
10.1152/ajprenal.1994.266.6.F934Scopus ID
2-s2.0-0028284028 (requires institutional sign-in at Scopus site) 142 CitationsAbstract
The role of endogenous P-450 metabolites of arachidonic acid (AA) on the tubuloglomerular feedback (TGF) response was examined. Under control conditions stop-flow pressure (SFP) fell by 17.0 +/- 2.1 mmHg when the perfusion rate of the loop of Henle was increased from 0 to 50 nl/min. Addition of AA (50 microM) to the perfusate lowered basal SFP by 11.4 +/- 1.1 mmHg and potentiated the TGF response. This effect was blocked by addition of a P-450 inhibitor, 17-octadecynoic acid (17-ODYA) (10 microM), to the perfusate. Perfusion of the loop of Henle with 17-ODYA elevated basal SFP by 3.7 +/- 0.3 mmHg and reduced the TGF response by 80%. After blockade of endogenous P-450 activity with 17-ODYA, addition of 20-hydroxyeicosatetraenoic acid (20-HETE, 10 microM) to the perfusate produced a flow rate-dependent fall in SFP. The effect of 20-HETE was not altered by pretreating the animal with meclofenamate (2 mg/kg iv) or by perfusing the nephron segment with furosemide (50 microM). These results indicate that endogenous P-450 metabolites of AA, particularly 20-HETE, may play a role in TGF and the regulation of renal vascular tone.
Author List
Zou AP, Imig JD, Ortiz de Montellano PR, Sui Z, Falck JR, Roman RJMESH terms used to index this publication - Major topics in bold
AnimalsArachidonic Acid
Cytochrome P-450 Enzyme System
Feedback
Furosemide
Hydroxyeicosatetraenoic Acids
Kidney Glomerulus
Kidney Tubules
Male
Meclofenamic Acid
Mixed Function Oxygenases
Osmolar Concentration
Perfusion
Pressure
Rats
Rats, Sprague-Dawley
