Arsenic exposure decreases rhythmic contractions of vascular tone through sodium transporters and K+ channels

Figure 1 Putative model of arsenic effect on vasomotion phenomenon in blood vessels. The figure shows the stimulation of the Na⁺/K⁺-ATPase by endothelial nitric oxide (NO) and stimulation of the Na⁺-K⁺-2Cl^- cotransporter by endothelial prostaglandins (PG). Arsenic would reduce NO bioavailability or would increase PG level, both of them would produce an increase in vasoconstriction or a decrease in the repolarization of the cell membrane, respectively, and then would reduce vasomotion. PE: Phenylephrine; As: Arsenic; eNOS: Endothelial nitric oxide synthase; SR: Sarcoplasmic reticulum.