Taken together, these data indicate that Sp1 and Sp3 deletion abolished the captopril-induced alleviation of endothelial dysfunction and the anti-apoptotic effects of captopril in endothelial cells; Sp1 and Sp3 have an indispensable role in the success of captopril treatment in the endothelium. This evidence concerns the gene SP1 and endothelial dysfunction.