Why the study?
Does inhibition of NHE-1 activity prevent increased intracellular Na+ and induce regression of cardiac hypertrophy in experimental models?
Does inhibition of NHE-1 activity prevent increased intracellular Na+ and induce regression of cardiac hypertrophy in experimental models?
Inhibition of the Na+/H+ exchanger 1 (NHE-1) represents a potential therapeutic target for reversing cardiac hypertrophy and treating heart failure in experimental models.
O verload of neonatal and adult cardiomyocytes and mul- ticellular myocardial preparations, which include whole hearts, are accompanied by an enhanced activity of the Na /H exchanger 1 (NHE-1). Exogenous administration of prohypertrophic agents such as angiotensin II (Ang II), endothelin-1 (ET-1), and 1 -adrenergic agonists also stimulates NHE-1 activity, which leads to an increased concentration of intracellular Na ([Na ] i ). Moreover, inhibition of NHE-1 activity prevents the increase in [Na ] i , induces the regression of cardiac hypertrophy, and exerts beneficial effects in experimental heart failure.
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Cingolani et al. (2007) studied this question.
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