الفهرس 
ACKNOWLEDGMENTOnly 14 pages are availabe for public view
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Abstract
Hypertension is a common health issue resulting in serious complications and it is considered as a silent killer. Treatment of hypertension represents a clinical challenge as its pathophysiology isn’t clear and many theories emerged over years to explain its pathogenesis. The positive feedback loop between oxidative stress, inflammation and endothelial dysfunction is accused of being one of the key players in the development of hypertension, vascular remodeling and its related complications. Oxidative stress and vascular inflammation are closely interrelated and both lead to endothelial dysfunction. The resultant endothelial dysfunction and vascular damage cause a pro-inflammatory condition and form a positive feedback loop. ROS decrease the production and bioavailability of NO resulting in impaired endothelial-dependent relaxation and elevation of ABP. In addition, oxidative stress increases the endothelial expression of CAMs such as VCAM-1, which is required for the recruitment and attachment of inflammatory cells. H2S is a gasotransmitter gained a great importance in the past decade due to its great therapeutic potentials. H2S is a strong anti-oxidant and anti-inflammatory agent. It has an anti-tumor and pro-angiogenic activity. H2S is considered a regulator of vascular tone through its effect on ion channels and endothelial NO. Moreover, it has a cardioprotective effects in case of ischemic injury. The crosstalk between H2S and NO plays an important role in maintenance of vascular tone and any defect in H2S/NO homeostasis contributes in the pathogenesis of hypertension. H2S affects the bioavailability of NO and NO influences the production of H2S and many physiological actions of H2S are mediated and enhanced by NO. So the aim of this work was designed to evaluate the possible role of H2S in the prevention of hypertension and its possible effects on the inflammatory process, oxidative stress, and vascular remodeling in L-NAME-induced hypertensive rats. The study included forty male Wistar Albino rats, which were assigned into four groups; the control group, the H2S control group, the hypertensive group, and the treated group receiving concomitant treatment with NaHS and L-NAME. ABP was measured and mean ABP was calculated. Serum levels of NO, total peroxide and TAC were measured and OSI was calculated. Aortae were harvested and aortic weight, length and aortic weight/length ratio were determined. Aortic fold expression of IFN-γ and VCAM-1 mRNA were measured using q-PCR. Aortic diameter, media thickness and elastin content were measured morphometrically.