High-salt diet is known to result in attenuation of endothe- lium-dependent relaxation in rat aorta. We investigated the possible alterations in electrical responses of rat aortic endot- helial cells to acetylcholine as one of the eventual mechanisms that lead to inhibition of endothelium-dependent relaxation induced by high-salt diet. It was shown that endothelial resting membrane potential in rats fed by high-salt diet did not differ significantly from that observed in the control group (–40,6±2,3 mV and –41,2±0,9 mV, respectively). The amplitude of ace- tylcholine-induced hyperpolarization of endothelial cells in rats fed by high-salt diet was significantly attenuated (9,0±1,5 mV vs 22,7±1,3 mV in the control group). The amplitude of hyperpolarization increased to 25,7±1,3 mV when high-salt diet was administered with enalapril, the angiotensin-converting enzyme inhibitor. We conclude that high-salt diet leads to at- tenuation of hyperpolarization of rat aortic endothelial cells in response to acetylcholine, that may mediate inhibition of NO synthesis and endothelium-dependent relaxation. Angiotensin- converting enzyme inhibitor enalapril prevents the observed alterations in endothelial electrical responses induced by high- salt diet.