[Effect of inhibiting protein kinase C on calcium sensitivity of contractile apparatus of vascular smooth muscle during vasospasms of different origins].

The aim of the study was to investigate the role of protein kinase C (PKC) in changes in myofilament Ca(2+)-sensitivity of vascular smooth muscle cells (SMC) in rats at different vasospastic states: hypoxic pulmonary vasoconstriction, genetically determined hypertension, and hypertension resulted from ionizing radiation. All vasospastic states demonstrated rightward shifts in pCa-tension curves suggesting that myofilament Ca(2+)-sensitivity had increased. In chemically (beta-escin) skinned pulmonary artery, hypoxia-induced increase in myofilament Ca(2+)-sensitivity was completely abolished by PKC inhibitor chelerythrine. The similar results were demonstrated in skinned aorta SMC of spontaneously hypertensive rats where an increase in myofilament Ca(2+)-sensitivity was also abolished by PKC inhibitors chelerythrine and staurosporine. The chelerythrine partially inhibited myofilament Ca(2+)-sensitivity that had increased following gamma-radiation. The data suggest the key role of PKC activity in modulation of myofilament Ca(2+)-sensitivity in SMC. We conclude that PKC-mediated increase in myofilament Ca(2+)-sensitivity is one of the main mechanisms which contribute to the vasospasm of different genesis.