期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 280, 期 3, 页码 H1066-H1074出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2001.280.3.H1066
关键词
cytochrome P-450 4A enzymes; cytochrome P-450 omega-hydroxylase; potassium channels; vascular smooth muscle; dibromododecynyl-methylsulfimide; 17-octadecynoic acid
资金
- NHLBI NIH HHS [HL-65289, HL-29587, R37 HL036279, HL-37374] Funding Source: Medline
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 Ca2+-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.
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