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Hypertension, Vol 21, 995-999, Copyright © 1993 by American Heart Association

ARTICLES

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

JW Osborn, BJ Provo, JS Montana 3d and KA Trostel
University of Minnesota, Department of Animal Science, St. Paul 55108.

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.

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