Cessation Restores Blood Pressure Levels and Endothelial Function Affected by Cadmium Exposure on Rats

Chronic cadmium exposure produces high blood pressure and endothelial damage; however, it is not known whether these effects could be reversed by interrupting the exposure to the metal. Therefore, we evaluate the systolic blood pressure (SBP) and vascular reactivity during and following chronic cadmium-exposure discontinuance. Rats received 100 mg.L^-1 cadmium chloride (CdCl₂) in the drinking water or tap water (Ct) for 30 days and/or tap water for 30 days more. The cadmium plasma content, blood pressure and vascular reactivity of isolated aorta were evaluated. Cadmium exposure increased cadmium plasma content, SBP and aorta contractile responses to phenylephrine, all reversed after suspending exposure. Endothelial removal and nitric oxide synthase (NOS) inhibition increased phenylephrine response both on control and Cd-discontinuation models. Cd-discontinuation group presented increased CAMKII and PKA protein expression, as peNOS^Ser1177. Superoxide dismutase (SOD) incubation reduced contractile response on control group, and catalase incubation enhanced the response to phenylephrine in this group. Meanwhile, both SOD2 and catalase protein expression were increased in Cd-cessation rats. Our findings provide evidence that increased SBP and endothelial dysfunction induced by Cd chronic exposure are reversed by suspending the metal exposure probably due to an improvement of antioxidant enzymes and eNOS function.