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

作　　者：Javier Palacios Chukwuemeka R Nwokocha Fredi Cifuentes 

机构地区：[1]Departamento de Ciencias Químicas y Farmacéuticas,Universidad Arturo Prat,Iquique 1110939, Chile [2]Department of Basic Medical Science,Physiology Section, University of The West Indies,Mona Kingston JMAKN, Jamaica [3]Experimental Physiology Laboratory,Instituto Antofagasta,Universidad de Antofagasta,Antofagasta 02800,Chile

出　　处：《World Journal of Pharmacology》2014年第2期18-23,共6页世界药理学杂志

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：Arsenic VASOMOTION Na^＋/K^＋-ATPase Na^＋-K^＋-2Cl^- K^＋ channels Nitric oxide PROSTAGLANDIN Vascular 

分 类 号：R135.1[医药卫生—劳动卫生] R541[医药卫生—公共卫生与预防医学]