Hypertension, Vol 19, 658-662, Copyright © 1992 by American Heart Association
JW Osborn and BJ Provo
To determine the extent to which baroreceptor function is a determinant of
salt-dependent hypertension, we studied the cardiovascular and renal
responses to increasing dietary sodium chloride in sinoaortic- denervated
(n = 9) and sham-denervated (n = 9) Sprague-Dawley rats. Rats were
instrumented with an arterial catheter for measurement of arterial pressure
and were individually housed for daily measurements of water intake, sodium
intake, urinary output, and urinary sodium excretion. Arterial pressure was
monitored daily over a 30-minute period by computer. After 3 days of
control measurements (0.4% sodium chloride diet), dietary sodium chloride
was increased to 8.0% for 21 days, followed by a 3-day recovery period
(0.4% sodium chloride). Ingestion of an 8.0% sodium chloride diet resulted
in a 20- to 25-fold increase in sodium intake and a fivefold increase in
water intake in both groups. In sinoaortic-denervated rats, arterial
pressure increased approximately 10 mm Hg on days 5-10, 20 mm Hg on days
11-18, and 30 mm Hg on days 19-21 of 8.0% sodium chloride. Arterial
pressure returned to control levels within the first 24 hours of the
recovery period. Elevated sodium intake had no significant effect on
arterial pressure in the sham-denervated group. Finally, there were no
significant differences between groups in urine output or urinary sodium
excretion at any time during the study. We conclude that a primary
impairment in the afferent limb of the arterial baroreceptor reflex results
in salt- dependent hypertension in the Sprague-Dawley rat.
ARTICLES
Salt-dependent hypertension in the sinoaortic-denervated rat
University of Minnesota, Department of Veterinary Biology, St. Paul, Minn 55108.
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