Specifically, high glucose reduced the expression of TRPV1/eNOS and NO production, while activation of TRPV1 by capsaicin-mediated Ca2+ influx in endothelial cells can increase eNOS activity then stimulate NO production, which implies a novel mechanism underlying capsaicin-mediated amelioration of cardiomyopathy and endothelial dysfunction under diabetes condition. This evidence concerns the gene TRPV1 and cardiomyopathy.