Enhanced production of reactive oxygen species such as superoxide anion may contribute to arteriolar dysfunction, elevated vascular resistance, and organ damage in hypertensive individuals. Studies assessing the contribution of enhanced oxidative stress to altered microvascular function have demonstrated that dihydroethidine fluorescence and tetranitroblue tetrazolium dye reduction (indicators of oxidative stress) are significantly increased in arterioles and venules of spontaneously hypertensive rats and Dahl saltsensitive hypertensive rats on high-salt diet. This finding suggests that there is an enhanced production of oxygen free radicals in the microvasculature of hypertensive animals that could contribute to impaired relaxation in response to NO-dependent vasodilator stimuli or other vascular relaxation mechanisms, for example, prostacyclin-induced dilation. It also appears that elevated dietary salt intake alone can lead to an increase in oxidative stress in arterioles and resistance arteries of normotensive animals. As discussed next, alterations in the function of arterioles and resistance arteries due to the effects of high-salt diet alone may have important implications for the development of an elevated vascular resistance in salt-sensitive forms of hypertension.
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