Early hypertrophic signals after myocardial stretch. Role of reactive oxygen species and the sodium/hydrogen exchanger

HORACIO E. CINGOLANI; NÉSTOR G. PÉREZ; CLAUDIA I. CALDIZ; CAROLINA D. GARCIARENA; VERÓNICA C. DE GIUSTI; MARÍA V. CORREA; MARÍA C. VILLA-ABRILLE; ALEJANDRA M. YEVES; IRENE L. ENNIS; GLADYS CHIAPPE DE CINGOLANI; ERNESTO A. AIELLO

Mechanosensitivity in Cells and Tissues: Mechanosensitivy of the heart

Springer

Año: 2010; p. 327 - 371

In this chapter the enhanced activity of the cardiac Na+/H+ exchanger(NHE-1) after myocardial stretch is considered a key step of the intracellular signalingpathway leading to the slow force response to stretch as well as an early signalfor the development of cardiac hypertrophy.We propose that the chain of events triggeredby stretch begins with the release of small amounts of angiotensin II which inturn induce the release/formation of endothelin. The actions of these hormones triggerthe production of mitochondrial reactive oxygen species that enhances NHE-1activity, causing an increment in the intracellular Na+ concentration which promotesthe increase in intracellular Ca2+ concentration ([Ca2+]i) through the Na+/Ca2+exchanger. This [Ca2+]i increase would trigger cardiac hypertrophy by activationof widely recognized Ca2+-dependent intracellular signaling pathways.