Salt-sensitive hypertension caused by long-term α-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 -adrenergic antagonist prazosin was chronically Infiised 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 1® 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 Tor 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 (Hypertension 1993;21:995-999)