Inhibition of L-type calcium currents by salusin-β in rat cardiac ventricular myocytes

被引：21

作者：

Shi, Jing-Song ^{[1
]}

Li, Dong ^{[1
]}

Li, Ning ^{[2
]}

Lin, Li ^{[1
]}

Yang, Yong-Ji ^{[3
]}

Tang, Ying ^{[3
]}

Sun, Tao ^{[2
]}

Yuan, Wen-Jun ^{[1
,2
]}

Ren, An-Jing ^{[4
]}

机构：

[1] Second Mil Med Univ, Dept Physiol, Shanghai 200433, Peoples R China

[2] NingXia Med Univ, Dept Physiol & Neurobiol, Yinchuan 750004, Peoples R China

[3] Second Mil Med Univ, Dept Biophys, Shanghai 200433, Peoples R China

[4] Second Mil Med Univ, Dept Pathophysiol, Shanghai 200433, Peoples R China

来源：

PEPTIDES | 2010年 / 31卷 / 06期

基金：

中国国家自然科学基金;

关键词：

Calcium channel; Salusin-beta; Myocytes; Rat; POSTNATAL-DEVELOPMENT; CA2+; EXPRESSION; EXCHANGER; CELLS; HEART; CARDIOMYOCYTES; CHANNEL; ALPHA;

D O I：

10.1016/j.peptides.2010.03.016

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Salusin-beta is a new regulatory peptide relevant to the cardiovascular system and exerts negative inotropic effect on ventricular muscle. The purpose of the present study was to determine whether salusin-beta can inhibit cardiac L-type calcium channel current (I-Ca,I-L). Using whole-cell voltage-clamp techniques, I-Ca,I-L was measured in ventricular myocytes isolated from 12 to 16 weeks rats. Salusin-beta dose-dependently and reversibly reduced the magnitude of I-Ca,I-L in rat ventricular myocytes. Neither threshold potential nor the peak potential of current-voltage relationship was affected. Salusin-beta increased the rate of I-Ca,I-L inactivation without altering its gating properties. These results suggest salusin-beta inhibited I-Ca,I-L by increasing the rate of I-Ca,I-L inactivation and the inhibition of L-type Ca2+ channels induced by salusin-beta may contribute to its negative inotropic effect on ventricular muscle. (C) 2010 Elsevier Inc. All rights reserved.

引用

页码：1146 / 1149

页数：4

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