Key result
Endothelin-1 potentiated serotonin-induced contraction in the porcine coronary artery, involving the translocation and activity of PKC delta, but not PKC epsilon.
PKC delta, but not PKC epsilon, mediates the contractile potentiation by endothelin-1 in porcine coronary arteries.
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 (alpha, beta1, delta, and zeta) were identified but not PKC epsilon. Only PKC delta was translocated from the cytosolic to the membrane fraction during the contractile potentiation by ET-1. Our results suggest that the activity of PKC delta but not PKC epsilon is involved in the contractile strengthening by ET-1 in the porcine coronary artery.
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Obara et al. (2000) studied this question. Endothelin-1 was evaluated on Translocation of protein kinase C (PKC) from the cytosol to the membrane fraction. Endothelin-1 potentiated serotonin-induced contraction in the porcine coronary artery, involving the translocation and activity of PKC delta, but not PKC epsilon.
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