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.
A high-salt diet in rats has been shown to result in enhanced vasoconstrictor and/or reduced vasodilator responses of isolated arteries to agonists. The present experiments were designed to investigate the effects of dietary salt on the responses of the pressurized mesenteric resistance artery of the dog to constrictor and dilator agents. Dogs were fed diets containing three different levels of salt with sodium concentrations (in mmol/kg per day) of 0.4 (low salt; LS), 3.0 (intermediate salt; IS) and 6.0 (high salt; HS) for a period of 4 weeks. At the end of the feeding period, animals were killed and lengths of third-order mesenteric artery were obtained and mounted in a perfusion myograph and changes in internal diameter were measured using a microscope and video-tracking device. The responses to noradrenaline (NA), acetylcholine (ACh) and sodium nitroprusside (SNP) were then determined. The vasoconstrictor responses to NA were identical in the three groups. However, the relaxation response of the vessels to ACh was attenuated in HS dogs compared with LS dogs (P < 0.05), but not with IS dogs. The application of N(G)-nitro-l-arginine methyl ester, an inhibitor of nitric oxide synthase, reduced the relaxation responses to ACh comparably in all three groups. The relaxation responses of the vessels to SNP were similar in all groups. These results indicate that, in the dog mesenteric resistance artery, a high-salt diet does not affect vasoconstrictor responses to NA, but does attenuate the vasorelaxant action of ACh, largely by inhibiting the production of endothelium-derived relaxing factor.
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