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尿皮质素对成年大鼠心室肌细胞L型钙电流的影响。

Effect of urocortin on L-type calcium currents in adult rat ventricular myocytes.

作者信息

Tao Jin, Xu Hua'e, Yang Cui, Liu Chun-Na, Li Shengnan

机构信息

Department of Pharmacology, Nanjing Medical University, Nanjing 210029, China.

出版信息

Pharmacol Res. 2004 Nov;50(5):471-6. doi: 10.1016/j.phrs.2004.05.006.


DOI:10.1016/j.phrs.2004.05.006
PMID:15458766
Abstract

The newly isolated peptide, urocortin (UCN) has been found to have potent cardioprotective effects. In order to investigate the effect of UCN on L-type calcium currents (I(Ca,L)), exploring the mechanisms of UCN's cardioprotective effects, we directly measured the I(Ca,L) in the adult rat cardiac myocytes exposed to UCN using standard whole-cell patch-clamp recording technique. Our results showed that UCN exerted decreasing effects on the I(Ca,L) of the single adult rat cardiac myocytes. The current density was inhibited by about 35% after exposure of the cells to UCN (0.1 micromol L(-1)) for 10 min, from the control value of 7.19 +/- 1.44 pA/pF to 4.74 +/- 0.75 pA/pF (n = 5, P < 0.05). This I(Ca,L)-inhibiting action of UCN was concentration dependent. Moreover, no frequency dependence of UCN effects on I(Ca,L) was observed. In combination with previous reports, our results suggest that there might be a close relationship between the cardioprotective effects of UCN and L-type calcium channels.

摘要

新分离出的肽——尿皮质素(UCN)已被发现具有强大的心脏保护作用。为了研究UCN对L型钙电流(I(Ca,L))的影响,探索UCN心脏保护作用的机制,我们使用标准的全细胞膜片钳记录技术,直接测量了暴露于UCN的成年大鼠心肌细胞中的I(Ca,L)。我们的结果表明,UCN对单个成年大鼠心肌细胞的I(Ca,L)有降低作用。将细胞暴露于UCN(0.1微摩尔/升)10分钟后,电流密度从对照值7.19±1.44皮安/皮法抑制到4.74±0.75皮安/皮法(n = 5,P < 0.05),约被抑制35%。UCN的这种I(Ca,L)抑制作用呈浓度依赖性。此外,未观察到UCN对I(Ca,L)的作用有频率依赖性。结合先前的报道,我们的结果表明UCN的心脏保护作用与L型钙通道之间可能存在密切关系。

相似文献

[1]
Effect of urocortin on L-type calcium currents in adult rat ventricular myocytes.

Pharmacol Res. 2004-11

[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
[Effects of neuropeptide Y on ion channels in ventricular myocytes].

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引用本文的文献

[1]
Chondroprotection by urocortin involves blockade of the mechanosensitive ion channel Piezo1.

Sci Rep. 2017-7-11

[2]
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J Biol Chem. 2015-3-27

[3]
Post-conditioning protecting rat cardiomyocytes from apoptosis via attenuating calcium-sensing receptor-induced endo(sarco)plasmic reticulum stress.

Mol Cell Biochem. 2011-10-5

[4]
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Mol Cell Biochem. 2011-7-16

[5]
Calcium-sensing receptors regulate cardiomyocyte Ca2+ signaling via the sarcoplasmic reticulum-mitochondrion interface during hypoxia/reoxygenation.

J Biomed Sci. 2010-6-17

[6]
Post-conditioning protects cardiomyocytes from apoptosis via PKC(epsilon)-interacting with calcium-sensing receptors to inhibit endo(sarco)plasmic reticulum-mitochondria crosstalk.

Mol Cell Biochem. 2010-4-11

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