Abstract

Nitric oxide (No) is the most powerful vasodilator .Caveolin has been documented to inhibit eNOS and decrease the activity of NO. Hypertension is associated with an impaired endothelial function that includes reduced production and/ or NO release. Caveolin directly binds to eNOS, thereby regulating the NO production. Daidzein- A caveolin inhibitor by decrease caveolin activity, increase eNOS and NO production. In present study we fouced on NO pathway to further clarify the protective effect of Daidzein- in endothelium-dependent vasorelaxation in a Rat Model of DOCA-Salt-Induced Hypertension.
Methods: Wistar albino rats weighing 125–175 g (8–10 week old) are divided into (n= 6) in each group and purchased from animal house, I.S.F College of Pharmacy, Moga, Punjab, were employed in the present study. Hypertension was induced in sham control mice by uninephrectomy and deoxycorticosterone acetate (DOCA)-salt treatment (40 mg/kg.., s.c: 6 weeks, The model rats were randomly divided into five groups (n= 6) in each group, model (DOCA Salt 40mg/ kg for 6 weeks), Daidzein low dose (0.2mg/kg/day.,s.c 1 week), Daidzein high dose, ( 0.4 mg/kg/day s.c :1 week) and Lisinopril 1mg/kg., p.o., 1 week) following which all are scarified. Vascular endothelial dysfunction and expression of caveolin was analyzed.
Result: VED in hypertensive rats measured in terms of decreased reduced glutathione level, serum nitrite/nitrate conc. increased Ach-induced endothelium-dependent vasorelaxation. Our results demonstrate that daidzein reduces oxidative stress, prevents development and progression of hypertension by modulation of activated eNOS, endogenous antioxidants, serum NO.
Conclusion: Daidzein prevent development and progression of hypertension associated vascular endothelial dysfunction by decreasing eNOS expression and increasing NO production.