The eNOS Mutant Hypertensive Mouse Model​ refers to a genetically engineered mouse strain in which the gene for endothelial nitric oxide synthase (NOS3) is disrupted or deleted. This genetic modification leads to a systemic deficiency in nitric oxide (NO) production from the vascular endothelium, resulting in a reliable and stable hypertensive phenotype. The rationale behind this model stems from the critical role of the eNOS/NO pathway​ in cardiovascular homeostasis. eNOS enzyme in endothelial cells synthesizes NO, a potent gaseous signaling molecule that causes vasodilation, inhibits vascular smooth muscle cell proliferation, and prevents platelet aggregation and leukocyte adhesion. Disruption of this pathway is a fundamental mechanism underlying endothelial dysfunction and the development of hypertension in humans. Genetic Background:​ The knockout is typically maintained on a C57BL/6 background, but it has been backcrossed to others for specific studies. Method of Generation:​ The model is created by targeted disruption of the NOS3gene, preventing the functional expression of the eNOS protein.