A study on the mechanism of accelerated vascular injury induced by sodium loading

点击翻译按钮获取中文摘要

Background It is well known that an excessive intake of sodium is a risk factor for cardiovascular disease because it raises the blood pressure. However, sodium loading reportedly promotes cardiovascular disease independently of its effect on blood pressure. Methods and Results We examined the role of calcineurin in sodium loading-induced vascular inflammation using a wire injury model of the rat femoral artery. Calcineurin activity in the aorta was significantly higher in sodium-loaded normotensive rats such as Wistar Kyoto(WKY) and Dahl salt-resistant(DR) rats than that in control WKY and DR rats. Neointimal formation was also significantly enhanced in sodium-loaded WKY and DR rats as compared with control WKY and DR rats. Gene transfer of an adenovirus expressing a dominant-negative mutant of calcineurin(AdCalAΔC92Q) significantly suppressed neointimal formation in sodium-loaded WKY and DR rats to a level similar to that observed in control WKY and DR rats. Calcineurin activity and neointimal formation were more significantly enhanced in hypertensive rats, such as spontaneously hypertensive rats and sodium-loaded Dahi salt-sensitive rats ; AdCalAΔC92Q infection significantly suppressed neointimal formation in these rats. Conclusions These results suggest that sodium loading promotes vascular inflammation in normotensive and hypertensive rats and that calcineurin plays a pivotal role in this process.