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Results for “Polydipsia”

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At least 469 records · Page 26Linked to original sources
PubMed1969

Hyperphagia and polydipsia in socially isolated rhesus monkeys.

Three rhesus monkeys which had been isolated from social contact during their first year of life persistently overate and overdrank during adulthood. These monkeys ingested approximately twice as much fluid and food as the control animals reared normally.

Animals↗
PubMed1978

Lead exposure during infancy permanently increases lithium-induced polydipsia.

Lead (200 milligrams per kilogram) was administered daily by intubation to Long-Evans rats on days 3 through 30 of life. Thirty to 180 days after cessation of lead administration, the lead-treated rats were consistently more polydipsic after lithium administration (2 millimoles per kilogram per day) than were pair-treated controls. Lithium increased the plasma renin activity equally in both the lead treated and the control groups. These data are evidence that there may be permanent neural changes induced by postnatal exposure to lead that are manifested by pharmacological challenge with lithium.

Animals↗
PubMed1990

Converting-enzyme inhibition abolishes polydipsia induced by dietary NaCl and K depletion.

The present studies were designed to test the hypothesis that angiotensin II (ANG II) mediates nonosmotic thirst in animals fed the low-NaCl K-free diet by preventing the increased generation of ANG II using the converting-enzyme inhibitor, enalapril. Animals were fed either a control salt or low-NaCl K-free diet and were treated with or without enalapril. Water intake in rats fed the low-NaCl K-free diet increased more than twofold on day 3 and remained elevated over the 10-day period of study. Treatment with enalapril (40 mg.kg-1.day-1) 1) prevented the striking rise in plasma renin activity in rats fed the low-NaCl K-free diet, 2) led to complete blockade of the pressor response to a 50-ng injection of angiotensin I but not ANG II, 3) did not affect daily water intake in rats consuming the control salt diet, 4) did not reduce basal water intake in rats fed the low-NaCl K-free diet below values measured in control animals, and 5) did not abolish water intake in response to osmotic stimulation. However, enalapril treatment abolished the increase in water intake that occurs in animals fed the low-NaCl K-free diet. In a double crossover study using two groups of rats fed the low-NaCl K-free diet, enalapril prevented increased water intake in rats initially fed the low-NaCl K-free diet and rapidly inhibited increased water intake in rats fed the low-NaCl K-free diet after the high water intake had been established.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗