NNOS is involved in cardiac remodeling induced by chronic ethanol consumption.

Abstract

Chronic ethanol consumption has deleterious effects on the cardiovascular system by directly damaging the myocardial structure and/or by neurohormonal activation. Moreover, nitric oxide (NO) derived from neuronal NO synthase (nNOS) seems to be important to balance the harmful effects of ethanol consumption, because it influences several aspects of cardiac physiology and attenuates pathological cardiac remodeling. However, the impact of chronic ethanol consumption on nNOS expression is unknown. We address this subject in the present study by evaluating whether chronic ethanol consumption induces cardiac remodeling and hypertension, and if these changes are associated with alterations in the expression of nNOS. Male Wistar rats were examined after ingesting a 20% alcohol solution for 6 months. Blood alcohol concentration and brain natriuretic peptide (BNP) levels were measured. The cardiac remodeling was assessed by histomorphometric analysis and the nNOS expression was evaluated by immunofluorescence and western blot analysis. Our results show that chronic ethanol consumption induces cardiac remodeling, namely thinning of left ventricular wall, cardiomyocyte hypertrophy and increased fibrosis, and elevations of arterial blood pressure. They also show that in rats fed with ethanol for 6 months, the circulating BNP levels had decreased as well as the expression of nNOS in left ventricle cardiomyocytes. These findings suggest that the effects of chronic ethanol consumption on BNP levels and/or on nNOS expression in cardiomyocytes may contribute to aggravate the cardiac remodeling and leads to progression of cardiomyopathy.