Lack of association of NOS3 and ACE gene polymorphisms with coronary artery disease in Southern Tunisia

摘要

Endothelial nitric oxide synthase (eNOS, encoded by the NOS3 gene) synthesizes NO from L-arginine and molecular oxygen in vascular endothelial cells (Kind et al. 2009). Angiotensin-converting enzyme (ACE), present on the surface of vascular endothelial cells, generates the potent vasoconstrictor angiotensin II from angio-tensin I and inactivates the vasodilator bradykinin (Erdos 1990). Angiotensin II modulates NO synthesis in cardiovascular tissue, and NO modulates the action of angiotensin II (Dubey et al. 1995; Nakagami et al. 1999). Many polymorphisms located in the ACE and NOS3 genes have been reported to play a major role in the pathogenesis of coronary artery disease (CAD) and related outcomes (Cambien et 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 promoter activity and has been reported as a risk factor for coronary spasm in a Japanese population (Nakayama et al. 1999).