Abstract
Sodium nitrite (NaNO2) induces relaxation in isolated arteries partly through an endothelium-dependent mechanism involving NO-eNOS-sGC-cGMP pathway. The present study was designed to investigate the effect of chronic NaNO2 administration on arterial systolic blood pressure (SBP) and vascular function in hypertensive rats. NaNO2 (150 mg L−1) was given in drinking water for four weeks to spontaneously (SHR) and Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) treated hypertensive SD rats. Arterial SBP and vascular function in isolated aortae were studied. Total plasma nitrate/nitrite and vascular cyclic guanosine monophosphate (cGMP) levels were measured using commercially available assay kits. Vascular nitric oxide (NO) levels were evaluated by DAF-FM fluorescence while the proteins involved in endothelial nitric oxide synthase (eNOS) activation was determined by Western blotting. NaNO2 treatment reduced SBP, improved the impaired endothelium-dependent relaxation, increased plasma total nitrate/nitrite level and vascular tissue NO and cGMP levels in SHR. Furthermore, increased presence of phosphorylated eNOS and Hsp-90 was observed in NaNO2-treated SHR. The beneficial effect of nitrite treatment was not observed in L-NAME treated hypertensive SD rats. The present study provides evidence that chronic treatment of genetically hypertensive rats with NaNO2 improves endothelium-dependent relaxation in addition to its antihypertensive effect, partly through mechanisms involving activation of eNOS.
Highlights
Marker for Nitric oxide (NO) formation, it can be reduced back to NO by several enzymes and such reduction is enhanced by hypoxia[13,14,15]
These effects of in vivo sodium nitrite administration were not observed in Wistar Kyoto rats (WKY) rats, which, they are derived from genetically different sublines[19], are the conventional normotensive controls used for comparison with the SHR20–23
The present findings show that four weeks of sodium nitrite treatment successfully decreased the arterial blood pressure and improved endothelium-dependent relaxations in the Spontaneously Hypertensive Rats (SHR)
Summary
Marker for NO formation, it can be reduced back to NO by several enzymes and such reduction is enhanced by hypoxia[13,14,15]. It remains questionable whether or not endogenous nitrite contributes to vasodilatation under normal physiological conditions. Supplementation of sodium nitrite to genetically hypertensive animals causes a decrease in arterial blood pressure[16,17]. The present experiments were designed to investigate the effect of in vivo treatment with sodium nitrite on arterial blood pressure and endothelial dysfunction in two different model of hypertension and to examine the role of eNOS activation in the observed effects
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