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PubMed1977

Thirst following water deprivation in dogs.

Eight dogs were prepared with unilateral carotid loops, and trained to stand quietly in a modified Pavlov stand. They were deprived of water for 24 h, which significantly depleted both the cellular and extracellular fluid (ECF) compartments. When they were allowed access to water for 5 min, they promptly drank amounts sufficient to make up their fluid deficits. Infusion of water into the unilateral carotid loop to reduce the cerebral blood osmolality to normal did not consistently reduce drinking because of inadequate mixing in the Circle of Willis. The eight dogs were then prepared with bilateral loops and deprived of water. Infusion of water at 0.6 ml-kg-1-,min-1 reduced the jugular plasma osmolality to control levels but did not affect systemic osmolality and reduced the drinking by 72%. Intracarotid infusion of water at differing rates reduced drinking in a dose related fashion. Intravenous infusion of 0.15 M NaCl in an amount designed to expand the ECF volume to normal reduced drinking by 27%. Expansion of the ECF volume plus bilateral intracarotid infusion of water to remove the central osmotic stimulus completely inhibited drinking. It is concluded that drinking following water deprivation in dogs is controlled by both central osmotic and by extracellular fluid volume factors, and that the osmotic factor is the more important. The drinking stopped well before these fluid deficits, as judged by body fluid analysis, had been restored. Some other mechanisms, therefore, must be involved in satiety.

Animals↗
PubMed1978

Periventricular preoptic-hypothalamus is vital for thirst and normal water economy.

A midline stereotaxic lesion in rats destroying the periventricular tissue (lamina terminalis and preoptic-anterior hypothalamic periventricular stratum) surrounding the anteroventral third ventricle (AV3V) produces adipsia without other marked behavioral changes. Although food consumption is reduced in animals rendered adipsic by the lesion, feeding continued and intake is comparable to that of water-deprived-sham-lesioned animals. About half the rats recover drinking after a period of adipsia, but the others never resume water intake and become moribund. An analysis of urinary output indicates that adipsic animals fail to reduce urine volume and continue to elaborate an inappropriately dilute urine. The periventricular lesion-induced adipsia without compensating antidiuresis produces a significant rise in plasma protein, sodium, osmolality, and urea nitrogen which if untreated often results in acute encephalopathy leading to death. These data suggest that preoptic-anterior hypothalamic periventricular tissue houses vital neural elements which function in the modulation of water ingestive and conservation mechanisms directed at the maintenance of body fluid homeostasis.

Animals↗
PubMed1986

Volume influences on thirst and vasopressin secretion in dehydrated sheep.

The contribution of extracellular fluid volume (ECFV) to water consumption and plasma vasopressin concentration (PAVP) after water deprivation for 52 h was examined in sheep. Intravenous infusion of isotonic NaCl, equivalent to either estimated ECFV loss or total body water loss, significantly reduced water intake by 37% when water was offered 3 h after infusion but not when water was offered 1 h after infusion. Plasma osmolality (POsm) was reduced after 3 h. Infusion of 200 mM NaCl, which maintained POsm, decreased water consumption by the same degree as isotonic NaCl infusion. Thus large decreases in POsm had no effect on water intake in this experimental protocol. Lack of inhibition of drinking 1 h after infusion suggests that the decrease observed after 3 h may have been mediated by receptors in the interstitial fluid (ISF) compartment and not the intravascular compartment. PAVP was reduced 3 h after infusion of NaCl but not at 1 or 2 h after infusion. POsm was also decreased at 3 h. Thus reduction of PAVP by NaCl infusion may have been caused by either ISF or intracellular fluid volume expansion.

Animals↗
PubMed1990

Hypertonic and hypovolemic stimulation of thirst in pigs.

Young female pigs weighing from 15 to 45 kg were used. Plasma osmolality was slowly raised by an intravenous infusion of 15% NaCl. The behavioral threshold was when the pigs began to drink water, and the rise of osmolality was the stimulus. In 23 measurements on 8 pigs the rise of osmolality to initiate drinking was 10.4 +/- 1.4 mosmol/kg (mean +/- SE). There was also an estimated 3.8 +/- 1.4% rise of blood volume. Control infusions of 0.9% NaCl for 1 h usually resulted in no drinking, and plasma osmolality fell by 6.7 +/- 2.1 mosmol/kg, while blood volume did not change. Hypovolemia was effected using furosemide (1 mg/kg body wt) to cause excretion of nearly isotonic urine. Blood volume changes were estimated from plasma protein and packed cell volume data. In 28 measurements on 6 pigs, drinking occurred when blood volume had decreased by 6.7 +/- 1.8%. During 2-h control periods, blood volume did not change appreciably. Plasma osmolality decreased during both the furosemide treatment (by 3.5 +/- 0.7 mosmol/kg) and the controls (by 4.1 +/- 0.8 mosmol/kg).

Animals↗
PubMed1990

Effect of angiotensin-converting enzyme inhibitor on salt appetite and thirst of BALB/c mice.

The role of angiotensin II (ANG II) in Na-depletion-induced Na appetite of mice was investigated. Intraperitoneal injection of the angiotensin-converting enzyme inhibitor captopril at 1.7 mg/mouse (high dose) decreased the Na intake of the Na-depleted (furosemide-treated) mice by 80-85%. The decrease in Na intake was restored to the initial level by concurrent subcutaneous infusion of ANG II. High dose of captopril also decreased the Na intake of fluid-deprived, Na-depleted mice. High dose of captopril did not alter water intake in any of the four conditions examined, i.e., in fluid-replete, Na-depleted, water-deprived, or fluid-deprived, Na-depleted mice. Low dose of captopril (1.7 microgram/mouse) tended to or significantly enhanced Na intake of Na-depleted mice. Low dose of captopril, however, did not enhance water intake in any of the conditions examined. Both high- and low-dose captopril treatment decreased food intake in water-deprived mice, whether or not the mice were Na depleted as well. The addition of captopril (0.1 or 1.0 mg/ml) to the drinking water did not influence Na or food intake. Water intake was enhanced during treatment with the low but not with the high dose of captopril. The results are consistent with the proposition that ANG II is involved in the Na appetite of Na-depleted mice. ANG II does not appear to have a role in water intake of Na-depleted or water-deprived mice, but neural mechanisms in which angiotensin has a role may influence food intake of water-deprived mice.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Role of arteria baroreceptor input on thirst and urinary responses to intracerebroventricular angiotensin II.

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.

Angiotensin II↗
PubMed1995

Angiotensin II-induced thirst, but not sodium appetite, via AT1 receptors in organum cavum prelamina terminalis.

The angiotensin receptor specificity, with respect to fluid intake, of the organum cavum prelamina terminalis (OCPLT), a recently discovered discrete forebrain structure with high sensitivity to angiotensin II (ANG II), was investigated. ANG II (10 ng) microinjected into the OCPLT significantly increased water consumption but did not induce intake of a hypertonic (3%) NaCl solution. Losartan, an ANG II type 1 (AT1) receptor-specific antagonist, produced dose-related (1-100 ng) inhibition of ANG II-induced drinking. The ANG II type 2 receptor-specific antagonist CGP-42112A was ineffective. Intake of the 3% NaCl solution in response to microinjection of either of the antagonists into the OCPLT was never observed. These findings suggest that water intake produced by microinjection of ANG II into the OCPLT is mediated by AT1 receptors uniquely and that, in contrast to other regions of the brain, these receptors do not induce salt intake when stimulated by ANG II.

Angiotensin II↗
PubMed1999

Thermal dehydration-induced thirst in spontaneously hypertensive rats.

Spontaneously hypertensive (SH) rats and normotensive Wistar-Kyoto (WKY) rats were exposed to either 25 or 37.5 degrees C for 3.5 h, and their thermal and water balance responses were compared. After exposure, either a blood sample was obtained or the rats were allowed to rehydrate for 4 h. SH rats had both higher core temperatures and evaporative water losses during heat exposure. Measurements of hematocrit, hemoglobin concentration, plasma protein and sodium concentrations, and plasma osmolality indirectly showed that the SH rats were dehydrated relative to the WKY rats after exposure to either 25 or 37.5 degrees C. SH rats drank significantly more water but also had significantly higher urine volumes than the WKY rats and thus rehydrated only slightly better than the WKY rats. SH and WKY rats had similar levels of water intake and urine output after 24 h of water deprivation. The elevated thermal response of SH rats to heat exposure does not appear to lead to uncompensatable changes in body water status.

Animals↗
PubMed2001

Effects of hypotension and fluid depletion on central angiotensin-induced thirst and salt appetite.

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 microg x kg(-1) x min(-1)) 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.

Angiotensin II↗
PubMed1991

Thirst and salt appetite in horses treated with furosemide.

When a preliminary experiment in sodium-replete ponies revealed an increase, but not a significant increase, in salt consumption after furosemide treatment, the experiment was repeated using sodium-deficient horses in which aldosterone levels might be expected to be elevated to test the hypothesis that a background of aldosterone is necessary for salt appetite. Ten Standardbred mares were injected intravenously with furosemide or an equivalent volume of 0.9% sodium chloride as a control to test the effect of furosemide on their salt appetite and blood constituents. Sodium intake and sodium loss in urine, as well as water intake and urine output, were measured and compared to determine accuracy of compensation for natriuresis and diuresis. Plasma protein and packed cell volume showed significant increases in response to furosemide treatment (F = 29.31, P less than 0.001 and F = 11.20, P less than 0.001, respectively). There were no significant changes in plasma sodium concentration or osmolality in response to the treatment (P greater than 0.05). The furosemide-treated horses consumed 126 +/- 14.8 g salt, significantly more than when they were given the control injection (94.5 +/- 9.8 g; t = 2.22, P = 0.05). In response to furosemide, horses lost 962 +/- 79.7 and consumed 2,170 +/- 5 meq sodium; however, compared with control, they lost 955 meq more sodium and ingested only 570 meq more sodium, so they were undercompensating for natriuresis. The furosemide-treated horses drank 9.6 +/- 0.8 kg of water, significantly more than when they received the control injection (6.4 +/- 0.8 kg; t = 6.9, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1972

Thirst.

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Amphetamine↗