Phthalates are one of the main constituents of plastic, reaching up to 40% of the total plastic weight, and their main function
is to impart fexibility/elasticity to polymers that would otherwise be rigid. Phthalates are known as endocrine disruptors,
since they can interfere with hormone homeostasis. Regarding the cardiovascular system, it was already shown the efects of
di-(2-ethylhexyl) phthalate (DEHP) exposure with signifcant changes in several calcium-handling proteins and an increase
in the blood pressure of mice ofspring, suggesting that DEHP leads to vasocontraction. However, the mechanisms involved
were not elucidated yet. The aim of this study is to analyse the involvement of calcium channels in the efects induced by
DEHP on vascular smooth muscle cells. Endothelium-denuded aorta artery rings were prepared from male Wistar rats and
incubated in an organ bath, and the whole-cell confguration of Patch Clamp technique was used to measure the activity of
L-type Ca2+ channels (LTCC) in A7r5 cells. Overall, DEHP caused relaxation on KCl-induced contraction at higher concentrations and inhibited the basal and BAY K8644-stimulated calcium current, indicating that this drug blocks LTCC. These
results suggest that DEHP induces relaxation on vascular smooth muscle cells due to the inhibition of calcium channels.

• Cardiovascular Response of Rat Aorta to Di‑(2‑ethylhexyl) Phthalate (DEHP) Exposure