It has been thought that sympathoexcitation is involved in the pathogenesis of salt-sensitive hypertension. However, only a few attempts have been made to directly measure sympathetic nerve activity during the development of salt-induced hypertension. In the present study, we tried to elucidate how sympathetic nerve activity was involved in the development of hypertension in Dahl salt-sensitive (DS) rats, by directly and continuously measuring renal (RSNA) and lumbar sympathetic nerve activity (LSNA) in the same animals during the development of salt-induced hypertension. Instruments were attached to the subject male DS and Dahl salt-resistant (DR) rats in order to record RSNA, LSNA and arterial pressure via telemetry. The experiment consisted of 3 time periods, a 3-day control, a 14-day 8% salt-diet loading, and a 7-day recovery period. Mean arterial pressure (MAP), RSNA, LSNA and heart rate (HR) were measured continuously and simultaneously throughout the experimental period. MAP increased sharply during the first 3 days after the onset of 8% salt loading, from 100 ± 1 mmHg to 126 ± 1 mmHg, then continued to increase gradually from the 4th to the 14th day of salt loading, reaching 141 ± 1 mmHg in the DS rats. RSNA and LSNA decreased slightly, but significantly (P<0.05), during the salt loading period, relative to the pre-salt loading level. HR decreased gradually throughout the experimental period. These data suggest that the progressive increases in MAP induced by the 8% salt loading may not be attributed to the changes in the RSNA, LSNA or HR. After cessation of the 8% salt loading, MAP decreased exponentially over the 7-day recovery period. RSNA increased significantly in a sustained fashion in DS rats after cessation of the salt loading, while it remained unchanged during the corresponding period in the DR rats. No differences were shown in the responses of LSNA and HR to the cessation of the salt loading in DS rats, compared with the DR rats. It is therefore likely that RSNA may sensitively response to the decrease in salt intake, while it is insensitive to the increase in salt intake. In summary, the present observations suggest that neither RSNA and LSNA may be critically involved in the early phase of hypertension development induced by 8% salt loading in Dahl salt-sensitive rats.