engleski

The influence of high salt intake on vascular responses of middle cerebral arteries to flow- induced dilation of Sprague-Dawley rats

Objective: Sprague-Dawley (SD) rats on high salt diet (HSD) remain normotensive and exhibit impaired relaxation responses to acetylcholine and hypoxia, as well as normotensive women on HSD, while there are no data of HSD effect on the flow- induced dilation (FID). The aim of the present study was to determine the effect of high salt intake on microvascular responses to flow-induced dilation in SD rats. Design and method: 19 male SD rats were divided in two groups: a) control group (N=10) and b) group of rats on HSD for 7 days (4% NaCl ; N=9). Prior to decapitation, rats were anesthetized with 75 mg/kg ketamine+2.5 mg/kg midazolam. Middle cerebral arteries were isolated and cannulated (DMT pressure myograph) for vascular reactivity measurements in response to stepwise increase in pressure (Δ10-Δ100), in the absence/presence of the NOS inhibitor L-NAME, COX- 1, 2 inhibitor indomethacin (INDO), selective inhibitor of microsomal CYP450 epoxidase activity MS-PPOH, and superoxide dismutase mimetic TEMPOL. To test differences among groups Two-way ANOVA was used, p<0.05 considered significant. Results: FID was reduced in HSD group at each pressure gradient, but significantly at Δ40, Δ60 (P<0.001) and Δ100 (P<0.05). The presence of L- NAME, INDO and MS-PPOH (independantly) significantly reduced FID in the control group at each pressure gradient (P<0.05) except Δ10. L- NAME and INDO reduced FID in HSD group, but L-NAME significantly reduces FID at Δ20 and Δ40 (P<0.05). The presence of TEMPOL restores FID in HSD group to control levels at pressure gradients Δ20-Δ100 (P<0.05), while in control group TEMPOL had no effect. Conclusions: These results demonstrate that: 1) High salt intake impaires vascular responses to FID ; 2) Reactive oxygen species - superoxide anion radical (O2-) may contribute to impaired FID in rats on high salt diet ; 3) Mechanisms of FID are different in control and HSD groups – while NO mediates FID in both groups of rats, metabolites of COX-1, 2, and EETs could also contribute to FID in control group of rats.

high salt diet; endothelium; flow mediated dilation

nije evidentirano