Study of Relationship between G894T Variant of Endothelial Nitric Oxide Synthase Gene and Acute Ischemic Stroke

Abstract

Acute ischemic Stroke is considered to be the second most common cause of mortality and third most common cause of disability all over the world (Lozano et al., 2012). Ischemic stroke (IS) accounts for 87% of total stroke type while the rest 13% is subjected to hemorrhagic stroke (HS) (Misra et al., 2017). Clinical and experimental evidence suggests a role for vascular dysfunction in IS pathogenesis, of which endothelium-derived nitric oxide (NO) plays a pivotal role in vascular protection (Saidi et al 2010). NO is a soluble gas with a very short half -life that is synthesized and released in a continuous fashion in our body and it is considered the most important molecule produced by the vascular endothelium (Tousoulis et al., 2012). It has many activities that play a major role in vascular homeostasis including vascular relaxation, inhibition of platelet and leukocyte adhesion to the vascular wall and inhibition of proliferation of smooth muscles. It is also protective against atherosclerotic changes (Rai et al., 2014). Synthesis of NO is mediated by the action of an enzyme NOS. It acts on Arginine to produce Citrulline and NO (Bisht, 2013). Impaired endothelium dependent vasodilation is a general attribute of atherosclerotic vessels,