The Anrep effect: 100 years later

被引:109
作者
Cingolani, Horacio E. [1 ]
Perez, Nestor G.
Cingolani, Oscar H. [2 ]
Ennis, Irene L.
机构
[1] UNLP, Fac Ciencias Med, Ctr Invest Cardiovasc, RA-1900 La Plata, Argentina
[2] Johns Hopkins Univ Hosp, Div Cardiol, Baltimore, MD 21205 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2013年 / 304卷 / 02期
关键词
angiotensin II; NHE1; slow force response; stretch; transactivation; SLOW FORCE RESPONSE; MINERALOCORTICOID RECEPTOR ACTIVATION; MITOCHONDRIAL PERMEABILITY TRANSITION; GROWTH-FACTOR RECEPTOR; RAT CARDIAC MYOCYTES; NA+-H+ EXCHANGE; ANGIOTENSIN-II; VENTRICULAR MYOCYTES; MYOCARDIAL STRETCH; IN-VIVO;
D O I
10.1152/ajpheart.00508.2012
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Cingolani HE, Perez NG, Cingolani OH, Ennis IL. The Anrep effect: 100 years later. Am J Physiol Heart Circ Physiol 304: H175-H182, 2013. First published November 16, 2012; doi:10.1152/ajpheart.00508.2012.-Myocardial stretch elicits a rapid increase in developed force, which is mainly caused by an increase in myofilament calcium sensitivity (Frank-Starling mechanism). Over the ensuing 10-15 min, a second gradual increase in force takes place. This slow force response to stretch is known to be the result of an increase in the calcium transient amplitude and constitutes the in vitro equivalent of the Anrep effect described 100 years ago in the intact heart. In the present review, we will update and discuss what is known about the Anrep effect as the mechanical counterpart of autocrine/paracrine mechanisms involved in its genesis. The chain of events triggered by myocardial stretch comprises 1) release of angiotensin II, 2) release of endothelin, 3) activation of the mineralocorticoid receptor, 4) transactivation of the epidermal growth factor receptor, 5) increased formation of mitochondria reactive oxygen species, 6) activation of redox-sensitive kinases upstream myocardial Na+/H+ exchanger (NHE1), 7) NHE1 activation, 8) increase in intracellular Na+ concentration, and 9) increase in Ca2+ transient amplitude through the Na+/Ca2+ exchanger. We will present the experimental evidence supporting each of the signaling steps leading to the Anrep effect and its blunting by silencing NHE1 expression with a specific small hairpin interference RNA injected into the ventricular wall.
引用
收藏
页码:H175 / H182
页数:8
相关论文
共 82 条
[1]   Endothelin-1 stimulates the Na+/Ca2+ exchanger reverse mode through intracellular Na+ (Na+i) -: Dependent and Na+i-independent pathways [J].
Aiello, EA ;
Villa-Abrille, MC ;
Dulce, RA ;
Cingolani, HE ;
Pérez, NG .
HYPERTENSION, 2005, 45 (02) :288-293
[2]   THE EFFECTS OF MUSCLE LENGTH ON INTRACELLULAR CALCIUM TRANSIENTS IN MAMMALIAN CARDIAC-MUSCLE [J].
ALLEN, DG ;
KURIHARA, S .
JOURNAL OF PHYSIOLOGY-LONDON, 1982, 327 (JUN) :79-94
[3]   Mechanisms underlying the increase in force and Ca2+ transient that follow stretch of cardiac muscle -: A possible explanation of the Anrep effect [J].
Alvarez, BV ;
Pérez, NG ;
Ennis, IL ;
de Hurtado, MCC ;
Cingolani, HE .
CIRCULATION RESEARCH, 1999, 85 (08) :716-722
[4]   Chronic inhibition of Na+/H+-exchanger attenuates cardiac hypertrophy and prevents cellular remodeling in heart failure [J].
Baartscheer, A ;
Schumacher, CA ;
van Borren, MMGJ ;
Belterman, CNW ;
Coronel, R ;
Opthof, T ;
Fiolet, JWT .
CARDIOVASCULAR RESEARCH, 2005, 65 (01) :83-92
[5]   Angiotensin II increases vascular and renal endothelin-1 and functional endothelin converting enzyme activity in vivo: Role of ETA receptors for endothelin regulation [J].
Barton, M ;
Shaw, S ;
dUscio, LV ;
Moreau, P ;
Luscher, TF .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1997, 238 (03) :861-865
[6]   Intracellular Na+ regulation in cardiac myocytes [J].
Bers, DM ;
Barry, WH ;
Despa, S .
CARDIOVASCULAR RESEARCH, 2003, 57 (04) :897-912
[7]   SARCOPLASMIC-RETICULUM IN CARDIAC LENGTH-DEPENDENT ACTIVATION IN RABBITS [J].
BLUHM, WF ;
LEW, WYW .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1995, 269 (03) :H965-H972
[8]   Mechanisms of length history-dependent tension in an ionic model of the cardiac myocyte [J].
Bluhm, WF ;
Lew, WYW ;
Garfinkel, A ;
McCulloch, AD .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1998, 274 (03) :H1032-H1040
[9]   Triggering mitochondrial radical release - A new function for NADPH oxidases [J].
Brandes, RP .
HYPERTENSION, 2005, 45 (05) :847-848
[10]   Angiotensin II (AT1) receptors and NADPH oxidase regulate Cl- current elicited by β1 integrin stretch in rabbit ventricular myocytes [J].
Browe, DM ;
Baumgarten, CM .
JOURNAL OF GENERAL PHYSIOLOGY, 2004, 124 (03) :273-287