用环匹阿尼酸、毒胡萝卜素和ryanodine排空细胞内钙库诱发兔主动脉的张力。

Evoked tensions in rabbit aorta by emptying intracellular Ca2+ stores with cyclopiazonic acid, thapsigargin, and ryanodine.

作者信息

Luo D L, Li W H

机构信息

Department of Pharmacology, Harbin Medical University, China.

出版信息

Zhongguo Yao Li Xue Bao. 1995 May;16(3):280-4.

PMID:7660829

Abstract

AIM

To study the increase of plasma membrane Ca2+ permeability in response to depletion of intracellular Ca2+ stores.

METHODS

In Ca(2+)-free medium, 2 selective inhibitors of sarcoplasmic reticulum (SR) Ca2+ pump ATPase, cyclopiazonic acid (CPA) and thapsigargin (Tha), and an activator of Ca(2+)-induced Ca2+ release channel (CICR), ryanodine (Rya), depleted intracellular Ca2+ stores sensitive to both caffeine and phenylephrine in rabbit aortic rings and caused sustained tensions when Ca2+ reintroduction. These tensions were taken as the increase of plasma Ca2+ permeability by depletion of intracellular Ca2+ stores.

RESULTS

The extracellular Ca(2+)-dependent tensions caused by Tha and Rya 3 mumol.L(-1) and CPA 30 mumol.L(-1) were 0.94, 1.1, and 0.14 g, respectively, and the tension caused by Rya was not inhibited by CPA.

CONCLUSION

(a) Besides the depletion of intracellular Ca2+ stores, an activated state of Ca2+ release channels in SR may also mediate the activation of Ca2+ influx from plasma membrane in rabbit aorta; (b) Rya needs caffeine to fully open CICR channel in SR.

摘要

目的

研究细胞内钙库耗竭时质膜钙通透性的增加情况。

方法

在无钙培养基中，两种肌浆网（SR）钙泵ATP酶的选择性抑制剂，环匹阿尼酸（CPA）和毒胡萝卜素（Tha），以及钙诱导钙释放通道（CICR）的激活剂，ryanodine（Rya），使兔主动脉环中对咖啡因和去氧肾上腺素敏感的细胞内钙库耗竭，并在重新引入钙时引起持续张力。这些张力被视为细胞内钙库耗竭导致的质膜钙通透性增加。