Effect of P-450 ω-hydroxylase metabolites of arachidonic acid on tubuloglomerular feedback

Ai Ping Zou, John D. Imig, Paul R. Ortiz De Montellano, Zhihua Sui, J R Falck, Richard J. Roman

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142 Scopus citations


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 μM) 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 μM), 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 μM) 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 μM). 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.

Original languageEnglish (US)
Pages (from-to)F934-F941
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Issue number6 35-6
StatePublished - Jun 1994


  • 17-octadecynoic acid
  • 20-hydroxyeicosatetraenoic acid
  • Afferent arteriole
  • Cytochrome P-450
  • Eicosanoids
  • Kidney
  • Renal hemodynamics

ASJC Scopus subject areas

  • Physiology


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