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1 Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112; 2 Department of Physiology, Medical College of Georgia, Augusta, Georgia 30912-2500; and 3 Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, Texas 75231
This study was conducted
to test the hypothesis that the cytochrome P-450 (CYP450)
metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) contributes to the
afferent arteriolar response to P2 receptor activation. Afferent
arteriolar responses to ATP, the P2X agonist, 
,
-methylene ATP and
the P2Y agonist UTP were determined before and after treatment with the
selective CYP450 hydroxylase inhibitor,
N-methylsulfonyl-12,12-dibromododec-11-enamide (DDMS) or the
20-HETE antagonist,
20-hydroxyeicosa-6(Z),15(Z)-dienoic acid
(20-HEDE). Stimulation with 1.0 and 10 µM ATP elicited an initial
preglomerular vasoconstriction of 12 ± 1% and 45 ± 4% and
a sustained vasoconstriction of 11 ± 1% and 11 ± 2%,
respectively. DDMS or 20-HEDE significantly attenuated the sustained
afferent arteriolar constrictor response to ATP. ,-Methylene ATP
(1 µM) induced a rapid initial afferent vasoconstriction of 64 ± 3%, which partially recovered to a stable diameter 10 ± 1%
smaller than control. Both DDMS and 20-HEDE significantly attenuated
the initial vasoconstriction and abolished the sustained
vasoconstrictor response to ,-methylene ATP. UTP decreased
afferent diameter by 50 ± 5% and 20-HEDE did not change this
response. In addition, the ATP-induced increase in the intracellular
Ca2+ concentration in preglomerular microvascular smooth
muscle cells was significantly attenuated by 20-HEDE. Taken together,
these results are consistent with the hypothesis that the CYP450
metabolite 20-HETE participates in the afferent arteriolar response to
activation of P2X receptors.
ATP; UTP; ,-methylene adenosine trisphosphate; afferent
arterioles; renal microcirculation; 20-hydroxyeicosatetraenoic acid
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