Several mechanism, including activation of the sympathetic nervous system, endothelin-mediated systemic vasoconstriction, impaired vasodilatation secondary to reduction in prostaglandin and nitric oxide, altered cytosolic calcium translocation, and activation of the renin-angiotensin system (RAS) have been proposed to underlie cyclosporine-induced hypertension [17]–[19]. This evidence concerns the gene REN and hypertensive disorder.