A low-protein diet (LPD) is known to affect the regulation of hemodynamics, and could contribute to the genesis of hypertension. We investigated the mechanism for the LPD-induced elevation of blood pressure in 52 Sprague-Dawley rats. Rats fed the LPD for 8 weeks showed a significantly higher blood pressure than those fed on a normal-protein diet (NPD) when the LPD included sucrose as a predominant component of carbohydrate (LPD with a high sucrose content, 135 +/- 2 mmHg; NPD, 124 +/- 2 mmHg; p<0.05). However, LPD with a low sucrose content, in which corn starch was the main component of carbohydrate, did not have a hypertensive effect (125 +/- 2 mmHg). Urinary epinephrine and norepinephrine excretion was significantly higher in the LPD high-sucrose group than in the NPD and LPD low-sucrose groups, and there was a significant positive correlation between urinary norepinephrine excretion and systolic blood pressure. Urinary nitric oxide excretion was no different between these groups, and 2 % L-arginine administration exerted no antihypertensive effect on the LPD-induced elevation of blood pressure. Sodium restriction also did not attenuate the LPD-induced elevation of blood pressure. These results suggest that the effect of LPD on blood pressure could be interpreted as the effect of the high sucrose content supplemented to the LPD rather than the direct effect of protein restriction, and that the stimulation of sympathetic nervous activity was associated with this elevation of blood pressure.