Abstract
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 language | English (US) |
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Pages (from-to) | F934-F941 |
Journal | American Journal of Physiology - Renal Fluid and Electrolyte Physiology |
Volume | 266 |
Issue number | 6 35-6 |
State | Published - Jun 1994 |
Keywords
- 17-octadecynoic acid
- 20-hydroxyeicosatetraenoic acid
- Afferent arteriole
- Cytochrome P-450
- Eicosanoids
- Kidney
- Renal hemodynamics
ASJC Scopus subject areas
- Physiology