ENHANCED MYOCARDIAL-FUNCTION IN TRANSGENIC MICE OVEREXPRESSING THE BETA(2)-ADRENERGIC RECEPTOR

被引：627

作者：

MILANO, CA

ALLEN, LF

ROCKMAN, HA

DOLBER, PC

MCMINN, TR

CHIEN, KR

JOHNSON, TD

BOND, RA

LEFKOWITZ, RJ

机构：

[1] DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710

[2] DUKE UNIV,MED CTR,HOWARD HUGHES MED INST,DURHAM,NC 27710

[3] DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710

[4] DUKE UNIV,MED CTR,DEPT PEDIAT,DURHAM,NC 27710

[5] UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093

[6] UNIV CALIF SAN DIEGO,CTR MOLEC GENET,LA JOLLA,CA 92093

[7] UNIV CALIF SAN DIEGO,AMER HEART ASSOC,BUGHER FDN CTR MOLEC BIOL,LA JOLLA,CA 92093

[8] BAYLOR COLL MED,DEPT ANESTHESIOL,HOUSTON,TX 77030

[9] UNIV HOUSTON,DEPT PHARMACOL,HOUSTON,TX 77030

来源：

SCIENCE | 1994年 / 264卷 / 5158期

关键词：

D O I：

10.1126/science.8160017

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Transgenic mice were created with cardiac-specific overexpression of the beta(2)-adrenergic receptor. This resulted in increased basal myocardial adenylyl cyclase activity, enhanced atrial contractility, and increased left ventricular function in vivo; these parameters at baseline in the transgenic animals were equal to those observed in control animals maximally stimulated with isoproterenol. These results illustrate a useful approach for studying the effect of gene expression on card iac contractility. Because oh ron ic heart failure in humans is accompanied by a reduction in the number of myocardial beta-adrenergic receptors and in inotropic responsiveness, these results suggest a potential gene therapy approach to this disease state.

引用

页码：582 / 586

页数：5

共 25 条

[1] SPECIFIC ATRIAL OVEREXPRESSION OF G-PROTEIN COUPLED HUMAN BETA(1)-ADRENOCEPTORS IN TRANSGENIC MICE [J].