Change in endothelial function in mesenteric arteries of Sprague-Dawley rats fed a high salt diet.

A high salt diet in some species results in elevated arterial blood pressure and alterations in vascular smooth muscle responses to agonists. Weanling male Sprague-Dawley rats were given either a high salt diet containing 8 % or a low salt diet of 0.4 % sodium chloride for a period of 4 weeks. At the end of the feeding period, tail systolic pressure was higher in the high salt than in low salt rats. The rats were then killed and the intestines removed. Vascular smooth muscle (VSM) responses were estimated from the changes in lumenal diameter of pressurised second order mesenteric resistance arteries. High salt diet resulted in enhanced VSM responses to noradrenaline. The vessels dilated in response both to acetylcholine and to sodium nitroprusside and the responses were similar in vessels from both high and low salt rats. However, vessels from high salt rats were resistant to the blocking of endothelium derived nitric oxide (EDNO) with L-NAME and the responses were instead abolished by blocking endothelium derived hyperpolarising factor (EDHF) with apamin and charybdotoxin. These results show that in Sprague-Dawley rats, a high salt diet enhances the vasoconstriction in response to noradrenaline. The vasodilatory responses to acetylcholine were not significantly changed. However, they appeared to be mediated mainly by EDHF rather than by EDNO as in the low salt animals.