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去甲肾上腺素在无细胞外钙情况下引起的大鼠主动脉收缩——II. 钙拮抗剂的作用

Norepinephrine-induced contractions of the rat aorta in the absence of extracellular calcium--II. Effects of calcium antagonists.

作者信息

Heaslip R J, Rahwan R G

出版信息

Gen Pharmacol. 1983;14(5):505-12. doi: 10.1016/0306-3623(83)90110-6.

DOI:10.1016/0306-3623(83)90110-6
PMID:6315527
Abstract

The rat aorta responds biphasically to norepinephrine (NE) in calcium-free medium, with the initial phasic and subsequent tonic components of the contraction being apparently mediated through mobilization of calcium from different intracellular pools. Membrane calcium channel blockers (verapamil, nifedipine, and SKF24260) did not affect the biphasic aortic contractions induced by NE in calcium-free medium, but reduced the response to NE in calcium-containing medium. Intracellular calcium antagonists (tertiary propyl and butyl methylenedioxyindenes) inhibited both phases of the NE-induced aortic contractions in calcium-free medium at concentrations which were similar to those required to inhibit NE-induced contractions in calcium-containing medium. These results support the concept that both components of the biphasic response of the rat aorta to NE are mediated through the mobilization of intracellular calcium when evoked in a calcium-free medium.

摘要

在无钙培养基中,大鼠主动脉对去甲肾上腺素(NE)产生双相反应,收缩的初始相和随后的强直相显然是通过从不同细胞内钙库中动员钙来介导的。膜钙通道阻滞剂(维拉帕米、硝苯地平和SKF24260)不影响无钙培养基中NE诱导的主动脉双相收缩,但降低了含钙培养基中对NE的反应。细胞内钙拮抗剂(叔丙基和丁基亚甲二氧基茚)在无钙培养基中抑制NE诱导的主动脉收缩的两个阶段,其浓度与抑制含钙培养基中NE诱导的收缩所需的浓度相似。这些结果支持这样一种观点,即当在无钙培养基中诱发时,大鼠主动脉对NE双相反应的两个组成部分都是通过细胞内钙的动员来介导的。

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引用本文的文献

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The mode of vasorelaxant action of 2-aminoisoquinoline, 1.3 (2H.4H)-dione, a novel 'intracellular calcium inhibitor'.新型“细胞内钙抑制剂”2-氨基异喹啉-1,3(2H,4H)-二酮的血管舒张作用模式
Br J Pharmacol. 1986 Feb;87(2):387-93. doi: 10.1111/j.1476-5381.1986.tb10828.x.
2
The effects of verapamil upon noradrenaline-induced contraction of the rat isolated aorta following acute and prolonged alterations in PO2.在急性和长期改变动脉血氧分压后,维拉帕米对去甲肾上腺素诱导的大鼠离体主动脉收缩的影响。
Br J Pharmacol. 1989 Dec;98(4):1101-8. doi: 10.1111/j.1476-5381.1989.tb12653.x.