Lack of Association of NOS3 and ACE Gene Polymorphisms with Coronary Artery Disease in Southern Tunisia

arginine and molecular oxygen in vascular endothelial cells (Kincl et al.2009). Angiotensin-converting enzyme (ACE), present on the surface of vascularendothelial cells, generates the potent vasoconstrictor angiotensin II from angio-tensin I and inactivates the vasodilator bradykinin (Erdo¨s 1990). Angiotensin IImodulates NO synthesis in cardiovascular tissue, and NO modulates the action ofangiotensin II (Dubey et al. 1995; Nakagami et al. 1999). Many polymorphismslocated in the ACE and NOS3 genes have been reported to play a major role in thepathogenesis of coronary artery disease (CAD) and related outcomes (Cambienet al. 1992; Yoshimura et al. 2000; Bor-Kucukatay et al. 2010; Hamelin et al. 2011).The -T786C polymorphism in the NOS3 gene causes a reduction of promoteractivity and has been reported as a risk factor for coronary spasm in a Japanesepopulation (Nakayama et al. 1999). The Glu298Asp polymorphism has been