Endothelin action: Inhibition by a protein kinase C inhibitor and involvement of phosphoinositols.
Endothelin action: Inhibition by a protein kinase C inhibitor and involvement of phosphoinositols.
复制标题
内皮素作用：蛋白激酶 C 抑制剂的抑制和磷酸肌醇的参与。
DOI：
10.1016/s0006-291x(89)80193-7
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发表时间：
1989
影响因子：
3.1
通讯作者：
Johns,JA
中科院分区：
文献类型：
--
作者：
Sugiura,M;Inagami,T;Hare,GM;Johns,JA
内皮素与兔主动脉条紧密结合，在细胞外Ca ~（2+）存在和不存在的情况下均引起长时间的血管收缩，尽管在后一种情况下仅产生部分收缩（20-30%），表明其作用可能不限于钙通道的开放。蛋白激酶C抑制剂1-（5-isoquinolynylsulfonyl）-2-甲基哌嗪（H-7）可逆转内皮素诱导的收缩。与Hirata等人（1）的观察结果相反，内皮素在培养的大鼠血管平滑肌细胞中引起强烈的磷脂酰肌醇分解，产生肌醇单磷酸、二磷酸和三磷酸。在相同的培养细胞中，它对环核苷酸水平没有影响。这些结果表明，磷脂酰肌醇周转和蛋白激酶C激活参与内皮素诱导的血管收缩。
Endothelin tightly bound to rabbit aortic strips and caused a prolonged vasoconstriction both in the presence and absence of extracellular Ca2+, although only partial constriction (20–30%) developed in the latter case, indicating that its action may not be limited to the opening of a calcium channel. The endothelin-induced constriction was reversed by the protein kinase C inhibitor, 1-(5-isoquinolynylsulfonyl)-2-methylpiperazine (H-7). In contrast to the observation of Hirata et al (1), endothelin caused a robust phosphatidylinositol breakdown producing inositol mono-, bis-and trisphosphates in cultured rat vascular smooth muscle cells. It showed no effect on cyclic nucleotide levels in the same cultured cells. These results indicate that phosphatidylinositol turnover and protein kinase C activation are involved in endothelin-induced vasoconstriction.