摘要
Arsenic-contaminated drinking water is a public health problem in countries such as Taiwan, Bangladesh, United States, Mexico, Argentina, and Chile. The chronic ingestion of arsenic-contaminated drinking water increases the risk for ischemic heart disease, cerebrovascular disease, and prevalence of hypertension. Although toxic arsenic effects are controversial, there is evidence that a high concentration of arsenic may induce hypertension through increase in vascular tone and resistance. Vascular tone is regulated by the rhythmic contractions of the blood vessels, generated by calcium oscillations in the cytosol of vascular smooth muscle cells. To regulate the cytosolic calcium oscillations, the membrane oscillator model involves the participation of Ca2+ channels, calcium-activated K+ channels, Na+/Ca2+exchange, plasma membrane Ca2+-ATPase, and the Na+/K+-ATPase. However, little is known about the role of K+ uptake by sodium transporters [Na+/K+-ATPase or Na+-K+-2Cl-(NKCC1)] on the rhythmic contractions.Vascular rhythmic contractions, or vasomotion are a local mechanism to regulate vascular resistance andblood flow. Since vascular rhythmic contractions of blood vessels are involved in modulating the vascular resistance, the blood flow, and the systemic pressure,we suggest a model explaining the participation of the sodium pump and NKCC1 co-transporter in low dose arsenic exposure effects on vasomotion and vascular dysfunction.
Arsenic-contaminated drinking water is a public health problem in countries such as Taiwan, Bangladesh, Unit-ed States, Mexico, Argentina, and Chile. The chronic in-gestion of arsenic-contaminated drinking water increas-es the risk for ischemic heart disease, cerebrovascular disease, and prevalence of hypertension. Although toxic arsenic effects are controversial, there is evi-dence that a high concentration of arsenic may induce hypertension through increase in vascular tone and resistance. Vascular tone is regulated by the rhythmic contractions of the blood vessels, generated by calcium oscillations in the cytosol of vascular smooth muscle cells. To regulate the cytosolic calcium oscillations, the membrane oscillator model involves the participation of Ca^2+ channels, calcium-activated K^+ channels, Na^+/Ca^2+ exchange, plasma membrane Ca^2+-ATPase, and the Na^+/K^+-ATPase. However, little is known about the role of K^+ uptake by sodium transporters [Na^+/K^+-ATPase or Na^+-K^+-2Cl^- (NKCC1)] on the rhythmic contractions. Vascular rhythmic contractions, or vasomotion are a local mechanism to regulate vascular resistance and blood flow. Since vascular rhythmic contractions of blood vessels are involved in modulating the vascular resistance, the blood flow, and the systemic pressure, we suggest a model explaining the participation of the sodium pump and NKCC1 co-transporter in low dose arsenic exposure effects on vasomotion and vascular dysfunction.
关键词
砷污染
心脏病
治疗方法
临床分析
Arsenic
Vasomotion
Na^+/K^+-ATPase
Na^+-K^+-2Cl^-
K^+ channels
Nitric oxide
Prostaglandin
Vascular