Myosin light chain phosphorylation plays an important regulatory role in Endothelin-1-induced contraction in coronary artery smooth muscle.
Endothelin-1 pathways in coronary smooth muscle remain preliminary; leaves open differential roles for MLC and caldesmon in human vasomotor disorders.
Endothelin-1 (ET), a potent vasoconstrictor, induces a sustained increase in the phosphorylation level of the 20-kDa myosin light chain (MLC) in porcine coronary artery strips. ET also induces late phosphorylation of caldesmon, which is mimicked by 12-deoxyphorbol 13-isobutyrate, but not by 60 mM KCl. Nitroglycerin, a vasorelaxant, completely reverses the ET-induced phosphorylation of MLC, but not that of caldesmon. These results suggest an important regulatory role of MLC phosphorylation in ET-induced contraction.
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Abe et al. (1991) studied this question.
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