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Departments of 1 Psychology, 3 Pharmacology, and 4 Exercise Science and 2 the Cardiovascular Center, University of Iowa, Iowa City, Iowa 52242-1407
We examined the
effects of hypotension and fluid depletion on water and sodium
ingestion in rats in response to intracerebroventricular infusions of
ANG II. Hypotension was produced by intravenous infusion of the
vasodilator drug minoxidil (25 µg · kg
1 · min1)
concurrently with the angiotensin-converting enzyme inhibitor captopril
(0.33 mg/min) to prevent endogenous ANG II formation. Hypotension
increased water intake in response to intracerebroventricular ANG II (30 ng/h) but not intake of 0.3 M NaCl solution and caused significant urinary retention of water and sodium. Acute fluid depletion was produced by subcutaneous injections of furosemide (10 mg/kg body wt) either alone or with captopril (100 mg/kg body wt sc)
before intracerebroventricular ANG II (15 or 30 ng/h) administration. Fluid depletion increased water intake in response to the highest dose
of intracerebroventricular ANG II but did not affect saline intake. In
the presence of captopril, fluid depletion increased intakes of both
water and saline in response to both doses of intracerebroventricular
ANG II. Because captopril administration causes hypotension in
fluid-depleted animals, the results of the two experiments suggest that
hypotension in fluid-replete animals preferentially increases water
intake in response to intracerebroventricular ANG II and in
fluid-depleted animals increases both salt and water intake in response
to intracerebroventricular ANG II.
minoxidil; captopril; rats; urine volume; water balance; sodium excretion; sodium balance
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