Does a low-salt diet exert a protective effect on endothelial function in normal rats?

Sodium restriction is often used as an adjunct in the treatment of conditio ns characterized by endothelial dysfunction, such as hypertension and heart or kidney disease. However, the effect of sodium restriction on endothelia l function is not known. Therefore, male Wistar rats were studied after a f ixed salt diet had been maintained (low-salt group: 0.05% NaCl, n = 10; nor mal-salt group: 0.3% NaCl, n = 10) for 6 weeks. Blood pressure and sodium e xcretion values were measured once a week. Subsequently the rats were kille d, the aorta was removed, and rings were cut. Endothelium-independent (sodi um nitrite (SN)) and endothelium-dependent (acetylcholine (ACh)) vasodilato r responses were assessed in the presence of indomethacin (a cyclo-oxygenas e inhibitor) and in the presence or absence of NG-monomethyl-L-arginine (L- NMMA; a competitive inhibitor of nitric oxide (NO) synthase). Endothelium-i ndependent vasodilatation was not different for the two salt groups. Endoth elium-dependent vasodilatation, on the other hand, was different. The respo nse to ACh was almost completely abolished by L-NMMA in the normal-salt gro up, whereas vasodilatation was partially preserved during L-NMMA in the low -salt group. Accordingly, the L-NMMA-sensitive contribution to ACh-dependen t vasodilatation was smaller in the low-salt group. Thus, salt restriction induced a non-NO and non-prostaglandin-dependent vasodilating pathway. By e xclusion this could be endothelium-derived hyperpolarizing factor, a pathwa y of vasculoprotective potential. Accordingly, the relative contributions o f the different vasoactive endothelial pathways were affected by salt intak e. Further research will be needed to clarify the nature and importance of this non-NO, non-prostaglandin-dependent pathway in the clinical setting as well.