Exposição por 7 dias ao cádmio promove aumento da pressão arterial e alteração da reatividade da aorta de ratos

Abstract

Studies have shown that Cadmium exposure is associated with important vascular changes, often related to increased blood pressure. However, it is not known whether the effects of exposure to low concentrations for a short period could promote vascular dysfunction, and what are the mechanisms involved in this process. The aim of this study was to describe the pressoric and vascular effects of 7-day exposure to ClCd2 in rats. For this, Wistar rats received drinking water (Ct) or 100 mg/L ClCd2 solution (Cd) via drinking water for 7 days. Weight, plasma cadmium concentration, systolic blood pressure (SBP) and aortic ring responses to vasoactive agents were analyzed. Even at low plasma concentration (1.66 ± 0.38 µg/L), the animals exposed to the metal showed an increase in SBP (141.5 ± 3.0 vs 128.7 ± 1.84 mmHg) and in the contractile response to Phenylephrine (Phe) in isolated aortic rings. Removal of vascular endothelium and inhibition of the enzyme nitric oxide synthase (NOS) through L-NAME (100 µM) similarly increased contraction to Phenylephrine. Despite this, there was an increase in the protein expression of peNOS Ser1177 and in the basal production of nitric oxide (NO). Removal of H2O2 through Catalase incubation (1000 U/ml-1) reduced the contractile response only in the Cd group, which showed lower expression of Catalase and increased basal production of H2O2. In Phe (1 µM) pre-contracted rings, Cd group showed a reduction in endothelium-dependent (ACh) and independent (SNP) relaxation when compared to Ct group. However, in KCl (60 mM) pre-contracted rings, the response to SNP was similar between groups. Together, the results demonstrate that 7 days of exposure to Cadmium lead to increased blood pressure and aortic contraction to Phe and reduced relaxation. These vascular effects seem to involve reduced Catalase antioxidant defense against H2O2, with probable reduced activation of potassium channels, balanced by an increase in eNOS activity.