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Endothelin-1 induces vasoconstriction in aortic cells indirectly via phosphatidylinositol hydrolysis, internal Ca2+ release, and nonselective cation channel opening, which depolarizes the membrane and activates L-type Ca2+ channels.
The vasoconstricting action of endothelin-1 (ET-1) is partly mediated by voltage-dependent L-type Ca2+ channels. Activation of the Ca2+ channels is indirect. ET-1 action involves (i) the hydrolysis of phosphatidylinositol and the release of Ca2+ from internal stores and (ii) the opening of a nonselective cation channel in the plasma membrane. The resulting depolarization triggers the activity of L-type Ca2+ channels.
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Renterghem et al. (1989) studied this question.
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