To clarify the mechanism of contractile strengthening by endothelin-1 (ET-1), we measured translocation of protein kinase C (PKC) from the cytosol to the membrane fraction in the porcine coronary artery. ET-1 potentiated the serotonin-(5-hydroxytryptamine, 5-HT) induced contraction without any additional increase in myosin light chain phosphorylation. Four PKC isoforms (α, β1, δ, and ζ) were identified but not PKCε. Only PKCδ was translocated from the cytosolic to the membrane fraction during the contractile potentiation by ET-1. Our results suggest that the activity of PKCδ but not PKCε is involved in the contractile strengthening by ET-1 in the porcine coronary artery.
Department of Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, Japan
Address correspondence and reprint requests to: Kazuo Obara, Department of Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Shizuoka City, Shizuoka 422-8526, Japan. E-mail: email@example.com
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