Salt-sensitive hypertension caused by long-term alpha-adrenergic blockade in the rat.

We conducted the present study to test the hypothesis that sympathetic responsiveness, rather than its absolute level of activity, is a determinant of salt-sensitive hypertension. Sprague-Dawley rats were instrumented for computerized recordings of arterial pressure and placed in metabolic cages. In one group (n = 10), the alpha 1-adrenergic antagonist prazosin was chronically infused throughout the experiment. A second group served as a vehicle control (n = 9). Mean arterial pressure, sodium and water intake, urine output, and urinary sodium excretion were measured for 3 control days (0.4% NaCl diet), followed by 10 days of increased dietary NaCl (8.0% NaCl) and a subsequent 3-day recovery period (0.4% NaCl). Plasma renin activity was measured on day 2 of 0.4% NaCl, days 2 and 9 of 8.0% NaCl, and day 2 of the recovery period. Control values for all variables were similar between groups. Increased dietary NaCl resulted in a gradually developing hypertension in prazosin-treated rats. By day 10 of the 8% NaCl diet, arterial pressure had increased significantly more in prazosin-treated (41 +/- 6 mm Hg) compared with vehicle (8 +/- 4 mm Hg) rats. There were no differences between groups for daily or cumulative sodium or water balances throughout the study. During 0.4% NaCl, plasma renin activity was similar in prazosin (2.9 +/- 0.8 ng/mL per hour) and vehicle (4.1 +/- 0.7 ng/mL per hour) groups and was equally suppressed during 8.0% NaCl. These results are consistent with the hypothesis that impaired adrenergic responsiveness, caused by prazosin infusion, is a determinant of salt-sensitive hypertension in the rat.