LAUSR

Objectives: To study the effect of high-sodium intake on functional vasodilatation of mesenteric small artery (MSA) in Dahl salt-sensitive (DS) rats. Methods: 24 8-week male DS rats were randomized into 4 groups and administrated with normal sodium (0.6% NaCl, NS group), low sodium (0.3% NaCl, LS group) and high sodium (8% NaCl, HS group) diet, and HS plus benazepril (10 mg/kg/d, HB group) treatment, respectively. MSA inner diameter recorded by GigaView high-speed camera was used to evaluate the acetylcholine (10 &mgr;g/kg, Ach)-induced vasodilatation in situ and in vivo. Full-Field Laser perfusion imaging (LPI) was taken to record video frame rate images of blood flow before and after Ach infusion. Results: After 6-week dietary intervention, compared with that in NS group, Ach-induced MSA vasodilatation in LS group increased (103.35 ± 24.46% vs. 58.26 ± 19.50%, P < 0.01), in HS group decreased (31.15 ± 17.88% vs. 58.26 ± 19.50%, P < 0.05) significantly, and was similar in HB group (57.96 ± 24.70% vs. 58.26 ± 19.50%). Meanwhile, the vasodilatation in HB group was greater than that in HS group (P < 0.05) (Fig. 1A). After Ach infusion, in comparison to NS group, MSA blood perfusion significantly increased in LS group (40.64 ± 9.00% vs 18.04 ± 10.95%, p < 0.05) and attenuated in HS group (5.62 ± 3.39% vs. 18.04 ± 10.95%, p < 0.05), with no difference in HB group (20.59 ± 10.76% vs. 18.04 ± 10.95%) (Fig. 1B). Ach-induced alteration of MSA blood perfusion was greater in HB group than that in HS group (P < 0.05). Conclusion: High sodium intake severely impaired functional vasodilatation of the small artery in DS rats, which could be ameliorated by benazepril. Our findings highlighted the significance of sodium restriction on arterial function and hypertension treatment.