Endogenous endothelin 1 mediates angiotensin II-induced hypertrophy in electrically paced cardiac myocytes through EGFR transactivation, reactive oxygen species and NHE-1
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- 作者：María V. Correa (1)
Mariela B. Nolly (1)
Claudia I. Caldiz (1)
Gladys E. Chiappe de Cingolani (1)
Horacio E. Cingolani (1)
Irene L. Ennis (1) - 关键词：Cardiac hypertrophy ; Ang II ; ET ; 1 ; EGFR transactivation ; NHE ; 1 ; ROS
- 刊名：Pfl篓鹿gers Archiv - European Journal of Physiology
- 出版年：2014
- 出版时间：September 2014
- 年：2014
- 卷：466
- 期：9
- 页码：1819-1830
- 全文大小：1,224 KB
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Mariela B. Nolly (1)
Claudia I. Caldiz (1)
Gladys E. Chiappe de Cingolani (1)
Horacio E. Cingolani (1)
Irene L. Ennis (1)
1. Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Calle 60 y 120 S/N, La Plata, 1900, Argentina - ISSN：1432-2013
文摘
Emerging evidence supports a key role for endothelin-1 (ET-1) and the transactivation of the epidermal growth factor receptor (EGFR) in angiotensin II (Ang II) action. We aim to determine the potential role played by endogenous ET-1, EGFR transactivation and redox-dependent sodium hydrogen exchanger-1 (NHE-1) activation in the hypertrophic response to Ang II of cardiac myocytes. Electrically paced adult cat cardiomyocytes were placed in culture and stimulated with 1?nmol?l-1 Ang II or 5?nmol?l-1 ET-1. Ang II increased ~45?% cell surface area (CSA) and ~37?% [3H]-phenylalanine incorporation, effects that were blocked not only by losartan (Los) but also by BQ123 (AT1 and ETA receptor antagonists, respectively). Moreover, Ang II significantly increased ET-1 messenger RNA (mRNA) expression. ET-1 similarly increased myocyte CSA and protein synthesis, actions prevented by the reactive oxygen species scavenger MPG or the NHE-1 inhibitor cariporide (carip). ET-1 increased the phosphorylation of the redox-sensitive ERK1/2-p90RSK kinases, main activators of the NHE-1. This effect was prevented by MPG and the antagonist of EGFR, AG1478. Ang II, ET-1 and EGF increased myocardial superoxide production (187?±-?%, 149?±-?% and 163.7?±-?% of control, respectively) and AG1478 inhibited these effects. Interestingly, Los inhibited only Ang II whilst BQ123 cancelled both Ang II and ET-1 actions, supporting the sequential and unidirectional activation of AT1, ETA and EGFR. Based on the present evidence, we propose that endogenous ET-1 mediates the hypertrophic response to Ang II by a mechanism that involves EGFR transactivation and redox-dependent activation of the ERK1/2-p90RSK and NHE-1 in adult cardiomyocytes.