High NaCl intake decreases both flow-induced dilation and pressure-inducedmyogenic tone in resistance arteries from normotensive rats: Involvement of cyclooxygenase-2

The effect of high NaCl diet on resistance arteries is not yet fully docume nted. In order to assess the effect of NaCl on myogenic tone and flow-induc ed dilation independent of arterial blood pressure change, we used normoten sive rats which did not develop hypertension upon high NaCl intake. Normote nsive Wistar Kyoto Rats received a high (8%) or a normal NaCl diet (0.4%). Mesenteric resistance arteries (150 mum, internal diameter) were cannulated in an arterio-graph to allow perfusion of arteries under controlled pressu re and flow. Pressure-induced myogenic tone was lower in the high NaCl grou p than in the control group. Cyclooxygenase inhibition with indomethacin an d (N-(2-cyclohexyloxy)-4-nitro-phenyl)-methanesulphonamide, 1 mu mol/l) NS 398 (specific cyclooxygenase-2 inhibitor) similarly decreased myogenic tone in rats fed high NaCl but had no effect in those fed a normal NaCl diet. F low-induced dilation was decreased in the high NaCl group. Inhibition of ni tric oxide synthesis with N-G-nitro-L-arginine methyl ester decreased flow- induced dilation in both groups. Indomethacin and NS 398 did not change flo w-induced dilation. As shown by immunofluorescence COX-2 was present in the endothelium of arteries from rats with a high NaCl diet but not in those f ed a normal NaCl diet. Thus, chronic high NaCl intake decreased both flow-i nduced dilation and myogenic tone in resistance arteries. The chronic high NaCl did not affect the participation of nitric oxide on flow-induced dilat ion, but induced the expression of cyclooxygenase-2, which participates in myogenic tone. These results suggest that high NaCl changes flow and pressu re mechanosensing processes and strengthen the hypothesis that sodium ions have an important role in both pressure and flow-mechanotransduction in vas cular cells.