PMID: 8606040Jun 1, 1995Paper

A protein kinase C with divalent cations contributes to thromboxane A2-induced contraction in rabbit vascular smooth muscle

Fukushima Journal of Medical Science
K YamamotoH Nakanishi

Abstract

We investigated the mechanism of contraction induced by a stable thromboxane A2 receptor agonist, STA2, in rabbit aortic smooth muscles. STA2 induced a long-lasting contraction which persisted for over 5 hours. This contraction was found to be potently inhibited by EDTA. In the presence of EGTA, STA2 was able to slowly contract muscle to a near maximum level, suggestive of an extracellular Ca(2+)-independent component in STA2 action. Inhibition of the STA2-induced contraction by EDTA was partially overcome by the addition of Mg2+. Ca2+ and Mn2+ were also effective in attenuating the inhibition. A phorbol ester, PDBu, an activator of PKC (protein kinase C), induced a long lasting contraction in a manner similar to that of STA2. PKC inhibitors, staurosporine and H-7, inhibited the lasting contractions induced by STA2 and PDBu. PKC inhibitors abolished STA(2)-induced contraction in the absence of extracellular Ca2+, suggesting that Ca(2+)-influx from the extracellular space as well as PKC activation are involved in STA(2)-induced contraction. ML-7, a myosin light chain kinase inhibitor, also inhibited the STA(2)-induced contraction, but it did not abolish the contraction in the absence of extracellular Ca2+. Furthermore, STA2 elic...Continue Reading

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