Na+/H+ exchanger and myocardial growth

CINGOLANI HE; ENNIS IL

Physiological Mini Reviews

Soc Argentina de Fisiología

Año: 2005 vol. 1 p. 1 - 3

The stretching of a papillary muscle induces a sudden and immediate rise in force (Figure 1A: from points a to b), due to an augmentation in myofilament Ca2+ responsiveness. During the next 10 to 15 minutes a progressive increase in force develops known as the ?slow force response? (SFR), that is due to a progressive increase in Ca2+ transient amplitude (Figure 1B). The source for this increase in Ca2+ transient remained obscure until we proposed a link between Ca2+ influx mediated by Na+/ Ca2+ (NCX) exchange in reverse mode and the activation of the Na+/H+ exchanger (NHE-1) caused by stretch;1-4 being the increase in the Ca2+ transient secondary to the increase in intracellular Na+ concentration ([Na+]i) (Figure 1D ?control?). It is known that the increase in [Na+]i can induce an increase in intracellular Ca2+ levels ([Ca2+]i) through the NCX either as a result of a decrease in Ca2+ efflux (decreased forward mode) or an increase in Ca2+ entry (increased reverse mode). The fact that after myocardial stretch there is no increase in diastolic [Ca2+]i1,5 as would be expected for a decrease in Ca2+ efflux, suggests that the reverse mode of NCX is the mechanism involved in the increase in Ca2+ transient.1The SFR, the increase in [Na+]i and the increase in Ca2+ transient can be abolished by blocking the Angiotensin II (Ang II) AT1 receptors with losartan (Figure 1C and 1D); the endothelin (ET) ETA receptors by BQ123 and by inhibition of the NHE-1.6