ABSTRACT
The pharmacological basis of isosorbide mononitrate (ISMN), a widely used drug for cardiovascular diseases, is that it is metabolized to nitric oxide (NO). However, NO is a double-edged sword that results in either beneficial or detrimental effect. Vascular injury is the common consequence of many cardiovascular diseases, but it is not determined whether ISMN influences the restoration of injured artery in vivo. Carotid artery injury was induced by electric stimulation in mice. Vasoconstriction and endothelium-dependent and -independent relaxation were recorded by a multichannel acquisition and analysis system. ISMN (10 mg/kg, p.o.) treatment for 1 week and 1 month had no effect on reendothelialization, histology and function of carotid artery injured by electric stimulation. L-arginine (500 mg/kg, p.o.) and Nomega-nitro-L-arginine methyl ester (L-NAME) (50 mg/kg, p.o.) treatment for 1 week did not affect the reendothelialization process, but L-NAME treatment induced neointimal hyperplasia and inhibited endothelium-dependent relaxation in electrically injured artery. These results suggest that supplement of exogenous or endogenous NO has no effect on the restoration of injured artery, but inhibition of endogenous NO induces neointimal hyperplasia in injured artery. ISMN treatment does not affect the restoration of injured artery.
