Rogério Faustino Ribeiro Júnior

TL;DR: Acute exposure to lead below the reference blood concentration increases systolic arterial pressure by increasing angiotensin II levels due to ACE activation, and offers further evidence that acute exposure tolead can trigger early mechanisms of hypertension development and might be an environmental risk factor for cardiovascular disease.

TL;DR: The results suggest that on initial stages of lead exposure, increased SBP is caused by the increase in plasma ACE activity, and this effect is accompanied by increased p-eNOS, iNOS protein expression and Na+/K+-ATPase functional activity.

TL;DR: Investigating the acute effects of 6 nM HgCl2 on endothelial function of aortic rings suggests that acute low concentration mercury exposure, occurring time to time could induce vascular injury due to endothelial oxidative stress and contributing to increase peripheral resistance, being a high risk factor for public health.

TL;DR: It is demonstrated that myocardial contractility and expression of key Ca2+ handling proteins were preserved in the early phase and reduced at long-term during OSHs deprivation.

TL;DR: In isolated hearts mercury treatment promoted contractility dysfunction as a result of the decreased NKA activity, reduction of NCX and SERCA and increased PLB protein expression, offering further evidence that mercury chronic exposure, even at small concentrations, is an environmental risk factor affecting heart function.