, 1973). Increased cardiovascular risk after mercury exposure has been reported, and both acute and chronic mercury exposure produces several toxic effects on the cardiovascular system. Acute mercury administration reduces arterial blood pressure (Rhee and Choi, 1989 and Rossoni et al., 1999) and myocardial contractility (Oliveira et al., 1994). Acute HgCl2 (5 mg/Kg) also produces cardiac systolic and diastolic failure, and pulmonary hypertension in vivo ( Rossoni et al., 1999). In left

ventricular papillary muscles, 0.5 and 1 μM HgCl2 increase force development ( Oliveira et al., 1994 and Assis et al., 2003) probably resulting from the inhibition of sarcolemmal Na+,K+-ATPase (NKA) ( Anner et al., 1992). At higher concentrations, mercury produces a Nutlin-3a chemical structure negative inotropism as a consequence of calcium

overload by reducing sarcoplasmic reticulum Ca2+-ATPase activity ( Hechtenberg and Beyersmann, 1991). The metal also reduces tetanic tension development and myosin ATPase activity ( Vassallo et al., 1999 and Moreira et al., 2003) at these concentrations. In Langendorff-perfused hearts, perfusion find more with high concentrations of mercury also reduces cardiac contractility, thereby decreasing isovolumic pressure development ( Rhee and Choi, 1989 and Massaroni et al., 1995). Attention has recently been focused on the cardiovascular toxic effects of chronic mercury exposure and its association with hypertension, carotid atherosclerosis, myocardial infarction and coronary heart disease (Salonen et al., 2000, Virtanen et al., 2005 and Houston, 2007). Different forms of mercury, such as HgCl2 and methyl mercury, have different actions and adverse outcomes when acutely or when higher doses are used. For chronic low dose exposure Plasmin the proximate toxic agent is most likely inorganic mercury (Rooney, 2007). Moreover, studies

reporting mercury effects resulting from chronic exposition are still scarce and the underlying mechanisms are not yet well explored. In order to adequately control amounts of mercury absorption, we developed an experimental model for controlled chronic exposure to low concentrations of HgCl2; such a model describes an endothelial dysfunction in aorta and mesenteric resistance arteries due to decreased NO bioavailability by increased NADPH oxidase-derived O2- (Wiggers et al., 2008). We then investigated whether the effects of chronic exposure to low concentrations of mercury also affects cardiac contractility by evaluating effects on arterial and ventricular pressures, isolated heart, NKA and myosin ATPase activities, expression of calcium handling proteins and changes in myocyte morphometry. Findings provide further evidence that chronic exposure to low doses of mercury, even at concentrations considered to be safe, is an environmental risk factor for heart function and cardiovascular disease.