Cardiac hypertrophy and remodelling: pathophysiological consequences and protective effects of melatonin

Abstract

This survey summarizes the limited findings related to the ability of endogenously produced and exogenously administered melatonin to modify the response of the heart musculature to pathological situations that are normally accompanied by hypertrophy of the cardiomyocytes and alterations in cardiovascular physiology. Whereas melatonin did not reduce left ventricular hypertrophy in spontaneously hypertensive rats or in nitric oxide-deficient hypertension, it did have other beneficial effects, e.g. it curtailed oxidative damage to the heart that resulted in an attenuation of left ventricular fibrosis. In contrast to the findings in hypertensive rats, melatonin administration was effective in overcoming cardiac enlargement resulting from induced hyperthyroidism or chronic hypoxia exposure. In addition, in these situations, melatonin also conferred protection against free radical-mediated damage at the level of cardiomyocytes. Collectively, the results of the publications summarized herein along with numerous other published reports on other aspects of cardiovascular physiology indicate that, when damage to the heart is a result of free radicals, melatonin is clearly protective. This is not unexpected considering the now well documented potent antioxidative actions of both melatonin and its metabolites. In general, melatonin improves cardiovascular physiology and heart function.