Abstract

Objectives Carbon dioxide(CO2) is one of the factors that affect the constriction and dilatation of smooth muscle cells. Cyclooxigenase(COX) catalyzes have important roles in inducing inflammatory responses and prostanoids, generated from arachidonic acid by COX-1 and COX-2, are involved in modulating of vascular tone. This study aimed to clarify the role of CO2 in regulating COX expression in vascular smooth muscle cells and elucidate its effects for vascular endothelial function. Methods A7r5 rat smooth muscle cells were maintained in Dulbecco's modified Eagle's medium, supplemented with 10% fetal bovine serum, at 37ºC in a 5% CO2 incubator. The cells were exposed to 10% and 20% CO2 for 24 h. The expression of COX-1 and COX-2 was subsequently evaluated by real time PCR, and cell viability was analyzed following exposure to 10% and 20% CO2. Results The expression levels of COX-2 were significantly reduced by concentration dependence in the vascular smooth muscle cells following exposure to 10% and 20% CO2, while no significant difference was found in those of COX-1 before and after exposure. Cell viability also decreased on the depending on the concentration of CO2. Conclusions These results suggested that exposure to CO2 may suppress the vasodilatation via the downregulation of COX-2 expression in vascular smooth muscle cells.

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