After mercury PKC inhibitor treatment no changes were observed for perimeter, length, width or area of myocytes. Regarding the evaluation in collagen content in mercury-treated animals compared with controls no changes were observed. Since 30 days mercury treatment with low doses did not produce morphological alterations our findings suggest that functional changes here described are

not consequence of morphological changes. Potential limitations of the study. In the present study, we used fluid-filled manometric system as a method for performing the hemodynamic experiments. If we compared the present results with those performed using microtip pressure transducers, we observed that the present values obtained with polyethylene catheter are lower when compared to those obtained with the microtip catheter (Zimmer and Millar, 1998). Results using the microtip catheter are commonly performed in anesthetized rats, thereby reducing differences with the fluid-filled catheters. Because the use of anesthesia changes hemodynamic parameters, we used the fluid-filled manometric system to perform the present experiments, keeping in mind both the catheter’s resonance ABT263 effect and dumping which this manometric system produces. In any case, as the same fluid-filled manometric system was

used to perform all experiments, we believe the present results to be acceptable. In summary, results presented herein suggest that controlled chronic exposure to small concentrations of inorganic mercury, leading to plasma levels similar to those found after

continuous occupational exposure, begins to affect heart function, eventhough several cardiovascular parameters, such as arterial Protein kinase N1 pressure and LVSP measured in vivo, are still within normal ranges. In perfused hearts, however, a negative inotropic effect was found resulting from reduction in NKA activity, NCX and SERCA expression and PLB increases, together with a percentage reduction in the magnitude of the β-adrenergic response. It is important to emphasize that, although functional changes are not showing differences in vivo, heart function is maintained by compensatory or adaptive mechanisms such as sympathetic activation and increased myosin ATPase activity. These results reinforce the relevance of human chronic occupational exposure to small mercury concentration as a risk factor for heart function. None declared. This study was supported by grants from “Ministerio de Ciencia e Innovación” (MCINN) (SAF 2009-07201),“Instituto de Salud Carlos III” ISCIII (Red RECAVA, RD06/0014/0011 and RD06/0014/0007) and Banco Santander Central Hispano, Spain, and by grants from “Coordenação de Aperfeiçoamento de pessoal de Nível superior” (CAPES), “Conselho Nacional de Desenvolvimento Científico e Tecnológico” (CNPq), “Fundação de Amparo à Pesquisa do Espírito Santo” (FAPES) and “Fundo Estadual de Ciência e Tecnologia” (FUNCITEC-39767531/07), Brazil.