The Na⁺ receptor that exists in the hepatoportal region plays an important role in postprandial natriuresis and the regulation of Na⁺ balance during NaCl load. Thus it would be considered that a dysfunction of the hepatic Na⁺ receptor might result in the elevation of arterial pressure under a condition of high NaCl diet. To elucidate this hypothesis, arterial pressure was continuously measured during three weeks of high NaCl diet (8% NaCl) in four groups of rats: (i) intact rats, (ii) rats with hepatic denervation (HD), (iii) rats with sinoaortic denervation (SAD), and (iv) rats with SAD+HD. During a 1-week normal NaCl diet period, there was no difference in arterial pressure among the four groups. A high NaCl diet had no influence on arterial pressure in intact or HD rats; however, it significantly increased by 11 ± 3 mmHg in SAD rats. The addition of HD to SAD had no synergistic effect on arterial pressure; i.e., in SAD+HD rats, mean arterial pressure increased by 13 ± 1 mmHg. In conclusion, sinoaortic baroreceptor, but not hepatic Na⁺ receptor, has a significant role in the long-term regulation of arterial pressure on a high NaCl diet.