Endothelin does not appear to exert its vasoconstrictor effects by acting primarily at the calcium antagonist binding sites associated with L-type calcium channels.
Endothelin vasoconstriction occurs independently of L-type Ca channel binding sites in vitro; leaves open alternative mechanisms in animal models.
The effect of endothelin, a potent vasoconstrictor polypeptide, on three types of calcium antagonist binding sites was examined, in rat cardiac membrane fragments. Endothelin 10 nM affected neither the affinity nor density of dihydropyridine binding sites. At concentrations of 10(-12)-10(-7) M, endothelin failed to displace bound (+)-[3H]-PN 200/110, (-)-[3H]-D888 and (+)-cis-[3H]-diltiazem. These results suggest that the calcium antagonist binding sites associated with L-type calcium channels are not the primary site of action of endothelin.
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Gu et al. (1989) studied this question.
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