RGD Reference Report - 20-HETE modulates myogenic response of skeletal muscle resistance arteries from hypertensive Dahl-SS rats. - Rat Genome Database

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20-HETE modulates myogenic response of skeletal muscle resistance arteries from hypertensive Dahl-SS rats.

Authors: Frisbee, JC  Roman, RJ  Krishna, UM  Falck, JR  Lombard, JH 
Citation: Frisbee JC, etal., Am J Physiol Heart Circ Physiol 2001 Mar;280(3):H1066-74.
RGD ID: 628478
Pubmed: PMID:11179048   (View Abstract at PubMed)

The present study determined the role of 20-hydroxyeicosatetraenoic acid [20-HETE; produced by omega-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 Ca(2+)-activated potassium (K(Ca)) 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 K(Ca) channels through a receptor-mediated process.



Objects referenced in this article
Strain SS/JrHsdMcwi null Rattus norvegicus

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