Abstract

Objective To investigate the effect of high sodium intake on the vasoconstrictive function of mesenteric small artery(MSA)in Dahl salt-sensitive(DS)rats. Methods Eight-week-old male DS rats were randomized into 4 groups and administrated with normal sodium(0.6%NaCl, NS group, n=8), lower sodium(0.3%NaCl, LS group, n=8), high sodium(8%NaCl, HS group, n=7)diet, and high sodium plus benazepril(10 mg·kg-1·d-1, HB group, n=6)treatment, respectively.After 6 weeks of dietary intervention, full-field laser perfusion imaging(LPI)and moorFLPI software were used to record blood flow and noradrenaline(NA, 10 μg/kg)-induced vasoconstriction in MSA.The diameter of MSA was recorded in situ and in vivo before and after NA injection by a high-speed camera with a microscope. Results After a 6-week dietary intervention, compared with that in NS group, NA-induced MSA vasoconstriction in HS group was significantly enhanced(34.90%±15.46% vs.18.34%±4.15%, P=0.01), while there was no difference between HS and HB group(P=0.46). The duration of vasoconstriction in LS group was significantly shorter than that in HS group [(16.4±1.8)s vs.(23.9±8.0)s, P=0.02]. Compared with that in NS group, NA-induced MSA blood perfusion in HS group significantly attenuated(33.50%±5.14% vs. 21.60%±6.16%, P 0.05), while greater in HS than that in LS group(45.74%±10.17% vs. 28.78%±6.21%, P=0.04). Conclusions High sodium diet enhanced the vasoconstrictive function of MSA in vivo, which could not be reversed by benazepril.The results addressed the important role of high sodium intake in the hyperresponsiveness of small artery to catecholamine in hypertension. Key words: High sodium intake; Salt-sensitive hypertension; Dahl salt-sensitive rats; Mesenteric arteries; Vasoconstriction

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