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1 Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226; and 2 Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, Texas 75390
The present study
determined the role of 20-hydroxyeicosatetraenoic acid [20-HETE;
produced by 
-hydroxylation of arachidonic acid via cytochrome
P-450 (CP450) 4A enzymes] in regulating myogenic activation
of skeletal muscle resistance arteries from normotensive (NT) and
hypertensive (HT) Dahl salt-sensitive (SS) rats. Gracilis arteries (GA)
were isolated from each rat and viewed via television microscopy, and
changes in vessel diameter with altered transmural pressure were
measured with a video micrometer. Under control conditions, GA from
both groups exhibited strong, endothelium-independent myogenic
activation. Treatment of GA with 17-octadecynoic acid (17-ODYA;
inhibitor of CP450 4A enzymes) did not alter myogenic activation in NT
rats, but impaired this response in HT animals. Treatment of GA from HT
rats with dibromo-dodecynyl-methylsulfimide (DDMS; inhibitor of 20-HETE
production) impaired myogenic activation, as did application of
20-hydroxyeicosa-6(Z),15(Z)-dienoic acid, an
antagonist for 20-HETE receptors. Application of iberiotoxin, a
Ca2+-activated potassium (KCa) channel
inhibitor, restored myogenic activation from HT rats treated with DDMS.
These results suggest that myogenic activation of skeletal muscle
resistance arteries from NT Dahl-SS rats does not depend on CP450,
whereas myogenic activation of these vessels in HT Dahl-SS rats is
partly a function of 20-HETE production, inhibiting KCa
channels through a receptor-mediated process.
cytochrome P-450 4A enzymes; cytochrome P-450
-hydroxylase; potassium channels; vascular smooth muscle; dibromo-dodecynyl-methylsulfimide; 17-octadecynoic acid
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