Paper Title
Reestablishing Effects of V2 Receptor Inhibitors on Hyperhomocysteinemia Propelled Endothelial Dysfunction in Wistar Rats

Abstract
The Endothelium has a weight of more than 1 kg and has an area greater than three metre square consisting of more than a several trillion cells in an average adult male human being. Endothelium Dysfunction is defined as a particular type of endothelial phenotype alteration with a concluding injury to the harmonising qualities of the endothelium membrane, primarily consisting of the endothelium dependent upholding of the vascular tone, hemostasis, and inflammation. The primary results of endothelial dysfunction are atherosclerosis, elevated inflammation and some other important coronary intrications. The method used by us for developing Hyperhomocysteinemia in order to induce endothelial dysfunction in Wistar rats, was by the usage of L-methionine as our induction agent, employing the hyperhomocysteinemia model. The processes causing endothelial dysfunction by hyperhomocysteinemia comprise of the upregulation of NADPH oxidase, Repression or the downregulation of Dimethylarginine dimethylamino hydrolaze(DDAH), Making of homocysteiene thiolactone and the self-oxidation of the homocysteine molecule. The V2R has been found to be located in the kidneys, fetal lung tissue and the endothelium. It is associated to the signaling system of adenylyl cyclaze, by the help of cAMP in the role of a secondary messenger here. Some findings have suggested that there is a major decrease of the von-willebrand factor (Vwf) from the V2R which is responsible for playing a critical role in the affixing of blood platelets to the endothelium which in turn causes the disturbance of the primary hemostasis. Keywords - Endothelium Dysfunction, Hyperhomocysteinemia, V2R, DDAH, Vwf, cAMP