ENDOTHELIAN ACTIVATES THE DIHYDROPYRIDINE-SENSITIVE, VOLTAGE-DEPENDENT CA-2+ CHANNEL IN VASCULAR SMOOTH-MUSCLE
ENDOTHELIAN ACTIVATES THE DIHYDROPYRIDINE-SENSITIVE, VOLTAGE-DEPENDENT CA-2+ CHANNEL IN VASCULAR SMOOTH-MUSCLE
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DOI：
10.1073/pnas.86.10.3915
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发表时间：
1989-05-01
影响因子：
11.1
通讯作者：
MASAKI, T
中科院分区：
文献类型：
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作者：
GOTO, K;KASUYA, Y;MASAKI, T
内皮素是近年来从猪血管内皮细胞和人血管内皮细胞中发现的一种有效的内皮来源的缩血管多肽。在此，我们提供了内皮素激活猪冠状动脉平滑肌二氢吡啶敏感的电压依赖性钙通道的证据。低剂量二氢吡啶钙通道阻滞剂尼卡地平可有效拮抗内皮素的血管收缩作用。在高K+去极化溶液中，内皮素可增强钙离子引起的收缩，显著增强全细胞膜片钳记录上的高阈值钙通道电流，并导致主要依赖细胞外钙离子的细胞内钙离子持续增加。这些发现表明，内皮素通过直接或间接激活电压依赖性钙通道而发挥其收缩血管的作用。
Endothelin is a potent endothelium-derived vasoconstrictor peptide recently characterized from porcine and human vascular endothelial cells. Here we provide evidence that endothelin activates the dihydropyridine-sensitive, voltage-dependent Ca2+ channel in porcine coronary artery smooth muscle. The vasoconstrictor action of endothelin is efficiently antagonized by low doses of the dihydropyridine Ca2+-channel blocker nicardipine. Endothelin augments the Ca2+-induced contraction in a high-K+ depolarizing solution, markedly enhances high-threshold Ca2+-channel current on the whole-cell patch clamp recording, and causes a sustained increase in the intracellular Ca2+ that is largely dependent on extracellular Ca2+. These findings suggest that endothelin exerts its vasoconstrictor effect by either directly or indirectly activating the voltage-dependent Ca2+ channel.