Hu L, Manning R D
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505, USA.
Am J Physiol. 1995 Jun;268(6 Pt 2):H2375-83. doi: 10.1152/ajpheart.1995.268.6.H2375.
The aim of this study was to determine the role of nitric oxide (NO) in the development of salt-induced hypertension in the Brookhaven strain of Dahl rats. Six- to seven-week-old conscious salt-sensitive (S) and salt-resistant (R) rats with indwelling arterial and venous catheters received low-, normal-, and high-sodium intakes sequentially over a 16-day period, and L-arginine was infused intravenously at 2 or 4 mg.kg-1.min-1 over this time. The S rats had an impaired NO production as evidenced by a decreased urinary nitrate plus nitrite excretion. The administration of the low or high dose of L-arginine increased the whole body NO production of the S rats to that of the control R rats, and the high dose of L-arginine prevented the shift of long-term pressure-natriuresis relationship, the elevation of arterial pressure, and the increase in salt sensitivity of arterial pressure in the S rats. The sodium and water balances were not different between the age-matched R and S rats. In conclusion, a continuous infusion of L-arginine prevented both the changes in the pressure-natriuresis relationship and the development of salt-induced hypertension in Dahl S rats.