Heparin inhibits the inositol 1,4,5-trisphosphate-dependent, but not the independent, calcium release induced by guanine nucleotide in vascular smooth muscle.

Heparin inhibits the inositol 1,4,5-trisphosphate-dependent, but not the independent, calcium release induced by guanine nucleotide in vascular smooth muscle.
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肝素抑制血管平滑肌中鸟嘌呤核苷酸诱导的肌醇 1,4,5-三磷酸依赖性钙释放,但不抑制独立钙释放。

DOI:
10.1016/s0006-291x(88)81141-0
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发表时间:
1988
影响因子:
3.1
通讯作者:
Somlyo,AP
Somlyo,AP
中科院分区:
生物学4区
文献类型:
--
作者:
Kobayashi,S;Somlyo,AV;Somlyo,AP

文献摘要

被引文献

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通过测定皂苷通透性的兔主动脉张力变化,测定肝素对细胞内钙离子释放的影响。肝素抑制(IC_(50)=5μg/ml)InsP3诱导的钙释放,但不抑制咖啡因诱导的Ca~(2+)释放。GTPγS诱导的钙释放的起始成分(InsP3依赖)也被肝素抑制,但不依赖InsP3的成分对肝素和普鲁卡因都有抵抗作用。这些结果支持G蛋白激活的钙释放机制的存在,这种机制不是由InsP3介导的,也不是由钙离子引起的。
The effects of heparin on the release of intracellular Ca2+, assessed by tension development in saponin-permeabilized rabbit main pulmonary artery, were determined. Heparin inhibited (IC50= 5μg/ml) inositol2+1,4,5-trisphosphate (InsP3)-induced, but not caffeine-induced, Ca2+release. The initial (InsP3-dependent) component of GTPγS-induced Ca2+-release was also inhibited by heparin, but the InsP3-independent component was resistant to both heparin and procaine. These results support the existence of a G protein activated mechanism of Ca2+release that is not mediated by InsP3or by Ca2+-induced Ca2+release.