Mechanism of reduced water intake in rats at high altitude

1981 ◽  
Vol 240 (3) ◽  
pp. R187-R191 ◽  
Author(s):  
R. M. Jones ◽  
C. Terhaard ◽  
J. Zullo ◽  
S. M. Tenney
Keyword(s):  
Polyethylene Glycol ◽  
Angiotensin Ii ◽  
Body Temperature ◽  
Diabetes Insipidus ◽  
Water Intake ◽  
Hypobaric Hypoxia ◽  
Reduced Body ◽  
Osmotic Stimulation ◽  
Reduced Water ◽  
Stimulation Of

Water intake was reduced during the 1st day of hypobaric hypoxia (inspired O2 pressure of 75 Torr) to 35-40% of the normoxic level in both normal rats (N) and rats with diabetes insipidus (DI). Analysis of water intake under graded saline loads at several inspired O2 levels (inspired O2 fractional concentrations of 0.105, 0.120, and 0.2095) indicated that hypoxia increased the threshold for osmotic stimulation of drinking without changing the sensitivity of the response in both N and DI rats. Nephrectomized N rats reduced water intake during hypoxia to 33% of the nephrectomized normoxic level of intake, and nephrectomized DI rats reduced intake to 47% of the nephrectomized normoxic intake. From these results it is concluded that reduced angiotensin II formation was not the factor responsible for reduced water intake during hypoxia. Polyethylene glycol-induced hypovolemia resulted in increased water intake during normoxia, but during hypoxia it was reduced to 29% of the normoxic rate. Reduced body temperature and hyperventilation were not the source of hypoxic attenuation of thirst. The mechanism may reside beyond the central integration of osmotic and nonosmotic information, or at the osmotic sensing mechanism itself.

Thirst and brain angiotensin in cattle

1992 ◽  
Vol 262 (2) ◽  
pp. R204-R210
Author(s):  
J. R. Blair-West ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
R. S. Weisinger
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Enzyme Inhibitors ◽  
Converting Enzyme ◽  
Preoptic Nucleus ◽  
Angiotensin I ◽  
Converting Enzyme Inhibitors ◽  
Median Preoptic Nucleus ◽  
Angiotensin I Converting Enzyme ◽  
Reduced Water

Cows that were normally hydrated or deprived of water were given intravenous or intracerebroventricular (icv) infusions of angiotensin I converting-enzyme inhibitors (CEI) or angiotensin II antagonists. Normally hydrated Na-deficient cows increased water intake in a dose-related manner in response to icv infusion of angiotensin I (n = 5). The response to 3 micrograms/h angiotensin I was abolished by concurrent icv infusion of the CEI captopril at 3 mg/h but not by intravenous infusion of captopril at 120 mg/h, which reduced Na appetite (n = 5). The icv infusion of captopril at 12 mg/h did not reduce the water intake of cows that were water restricted for 26.5 h (n = 4) or water restricted and Na deficient (n = 4). The icv infusion of the more lipophilic CEI ramipril at 3 mg/h (n = 7) did not reduce the water intake of normally hydrated or dehydrated cows but reduced the "need-free" intake of Na solution by dehydrated cows. The icv infusion of the nonpeptide antagonist Du Pont 753 at 3 mg/h (n = 7) reduced water intake in dehydrated cows. The results indicate that brain angiotensin may be involved in thirst in cattle. The data suggest that this brain angiotensin II may be formed by a pathway that does not include converting enzyme and that is sited inside the blood brain barrier, possibly in the median preoptic nucleus.

Intracerebroventricular infusion of angiotensin II increases water and ethanol intake in rats

1999 ◽  
Vol 277 (1) ◽  
pp. R162-R172 ◽  
Author(s):  
R. S. Weisinger ◽  
J. R. Blair-West ◽  
P. Burns ◽  
D. A. Denton
Keyword(s):  
Angiotensin Ii ◽  
Direct Effect ◽  
Water Intake ◽  
Indirect Effect ◽  
Taste Preference ◽  
Ethanol Solution ◽  
Ethanol Intake ◽  
Ang Ii ◽  
Intracerebroventricular Infusion ◽  
Stimulation Of

The influence of prolonged ingestion of ethanol on stimulation of water or ethanol intake by intracerebroventricular infusion of ANG II was evaluated in rats. Animals were maintained for 5–6 mo with either 10% ethanol solution or water as their only source of fluid. In both groups of rats, infusion of ANG II caused a large increase in water intake (7-fold) and a lesser increase in 10% ethanol intake (2-fold). The effect of ANG II on the volume of ethanol solution ingested, however, was inversely related to the concentration of the ethanol solution. As the concentration of ethanol solution was decreased, frequency and duration of drinking bouts increased. The intake of sweetened 10% ethanol solution or commercially produced wine during infusion of ANG II was similar to the intake of 10% ethanol and not related to taste preference. In conclusion, chronic consumption of ethanol solution did not appear to adversely effect ANG II stimulation of water intake. The intake of ethanol solution during infusion of ANG II was inhibited by a direct effect of ingested ethanol and/or by indirect effect from metabolized ethanol.

scholarly journals A hypothalamic circuit that controls body temperature

2017 ◽  
Vol 114 (8) ◽  
pp. 2042-2047 ◽  
Author(s):  
Zheng-Dong Zhao ◽  
Wen Z. Yang ◽  
Cuicui Gao ◽  
Xin Fu ◽  
Wen Zhang ◽  
...  
Keyword(s):  
Body Temperature ◽  
Gabaergic Neurons ◽  
Designer Drugs ◽  
Electrophysiological Recording ◽  
Strong Increase ◽  
Temperature Sensitive ◽  
Neural Pathways ◽  
Dorsomedial Hypothalamus ◽  
Reduced Body ◽  
Stimulation Of

The homeostatic control of body temperature is essential for survival in mammals and is known to be regulated in part by temperature-sensitive neurons in the hypothalamus. However, the specific neural pathways and corresponding neural populations have not been fully elucidated. To identify these pathways, we used cFos staining to identify neurons that are activated by a thermal challenge and found induced expression in subsets of neurons within the ventral part of the lateral preoptic nucleus (vLPO) and the dorsal part of the dorsomedial hypothalamus (DMD). Activation of GABAergic neurons in the vLPO using optogenetics reduced body temperature, along with a decrease in physical activity. Optogenetic inhibition of these neurons resulted in fever-level hyperthermia. These GABAergic neurons project from the vLPO to the DMD and optogenetic stimulation of the nerve terminals in the DMD also reduced body temperature and activity. Electrophysiological recording revealed that the vLPO GABAergic neurons suppressed neural activity in DMD neurons, and fiber photometry of calcium transients revealed that DMD neurons were activated by cold. Accordingly, activation of DMD neurons using designer receptors exclusively activated by designer drugs (DREADDs) or optogenetics increased body temperature with a strong increase in energy expenditure and activity. Finally, optogenetic inhibition of DMD neurons triggered hypothermia, similar to stimulation of the GABAergic neurons in the vLPO. Thus, vLPO GABAergic neurons suppressed the thermogenic effect of DMD neurons. In aggregate, our data identify vLPO→DMD neural pathways that reduce core temperature in response to a thermal challenge, and we show that outputs from the DMD can induce activity-induced thermogenesis.

EFFECTS OF THE TEMPERATURE OF THE ENVIRONMENT AND THE DRINKING WATER ON THE BODY TEMPERATURE AND WATER CONSUMPTION OF SHEEP

1962 ◽  
Vol 42 (1) ◽  
pp. 1-8 ◽  
Author(s):  
C. B. Bailey ◽  
R. Hironaka ◽  
S. B Slen
Keyword(s):  
Drinking Water ◽  
Body Temperature ◽  
Water Intake ◽  
Water Consumption ◽  
Environmental Temperature ◽  
The Body ◽  
Average Temperature ◽  
Subcutaneous Tissues ◽  
Environmental Temperatures ◽  
Reduced Water

Temperatures in the rumen, rectum, and subcutaneous tissues of four sheep receiving [Formula: see text] pounds of alfalfa hay per day were recorded at environmental temperatures of 15 °C. and −12 °C. The temperature of the drinking water was 20 °C. when the environmental temperature was 15 °C. and variously 0°, 10°, 20°, and 30 °C. during four different periods when the environmental temperature was −12 °C. At both environmental temperatures, the temperature in the rumen was higher than that in the rectum which, in turn, was higher than that in the subcutaneous tissues. The consumption of feed caused a transient increase in the temperature in the rumen and rectum while the consumption of water caused a transient decrease in the temperature in the rumen. A reduction in environmental temperature from 15 °C. to −12 °C. caused decreases in the temperatures in the rumen, rectum, and subcutaneous tissues, and reduced water intake from about 1600 to about 800 milliliters/day. At an environmental temperature of −12 °C., the temperature of the drinking water did not influence the amount of water consumed. It did, however, have an effect on body temperature because the average temperature in the rectum was slightly higher when the drinking water was 0 °C. than when it was 30 °C.

Osmoregulatory fluid intake but not hypovolemic thirst is intact in mice lacking angiotensin

2008 ◽  
Vol 294 (5) ◽  
pp. R1533-R1543 ◽  
Author(s):  
Michael J. McKinley ◽  
Lesley L. Walker ◽  
Theodora Alexiou ◽  
Andrew M. Allen ◽  
Duncan J. Campbell ◽  
...  
Keyword(s):  
Polyethylene Glycol ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Subfornical Organ ◽  
Salt Appetite ◽  
Neural Pathways ◽  
Daily Water Intake ◽  
Similar Dose ◽  
Central Origin ◽  
Supraoptic Nuclei

Water intakes in response to hypertonic, hypovolemic, and dehydrational stimuli were investigated in mice lacking angiotensin II as a result of deletion of the angiotensinogen gene (Agt−/− mice), and in C57BL6 wild-type (WT) mice. Baseline daily water intake in Agt−/− mice was approximately threefold that of WT mice because of a renal developmental disorder of the urinary concentrating mechanisms in Agt−/− mice. Intraperitoneal injection of hypertonic saline (0.4 and 0.8 mol/l NaCl) caused a similar dose-dependent increase in water intake in both Agt−/− and WT mice during the hour following injection. As well, Agt−/− mice drank appropriate volumes of water following water deprivation for 7 h. However, Agt−/− mice did not increase water or 0.3 mol/l NaCl intake in the 8 h following administration of a hypovolemic stimulus (30% polyethylene glycol sc), whereas WT mice increased intakes of both solutions during this time. Osmoregulatory regions of the brain [hypothalamic paraventricular and supraoptic nuclei, median preoptic nucleus, organum vasculosum of the lamina terminalis (OVLT), and subfornical organ] showed an increased number of neurons exhibiting Fos-immunoreactivity in response to intraperitoneal hypertonic NaCl in both Agt−/− mice and WT mice. Polyethylene glycol treatment increased Fos-immunoreactivity in the subfornical organ, OVLT, and supraoptic nuclei in WT mice but only increased Fos-immunoreactivity in the supraoptic nucleus in Agt−/− mice. These data show that brain angiotensin is not essential for the adequate functioning of neural pathways mediating osmoregulatory thirst. However, angiotensin II of either peripheral or central origin is probably necessary for thirst and salt appetite that results from hypovolemia.

INCREASED SODIUM APPETITE IN ADRENALECTOMIZED OR HYPOPHYSECTOMIZED RATS AFTERINTRACRANIAL INJECTIONS OF RENIN OR ANGIOTENSIN II

1980 ◽  
Vol 87 (1) ◽  
pp. 109-112 ◽  
Author(s):  
D. B. AVRITH ◽  
M. J. WISELKA ◽  
J. T. FITZSIMONS
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Preoptic Area ◽  
Test Session ◽  
Free Access ◽  
Initial Water ◽  
Sodium Appetite ◽  
Hypophysectomized Rats ◽  
Access To Food ◽  
Stimulation Of

Rats given free access to food, water and 2·7% NaCl and injected with either renin or angiotensin II into the preoptic area showed an immediate increase in water intake followed by an increase in intake of 2·7% NaCl. The rats continued to drink the hypertonic NaCl solution throughout the test session of 18 h. Intracranial injections of the dipsogen, carbachol, caused thirst but no sodium appetite. Bilateral adrenalectomy had no effect on either the initial water intake or the delayed intake of NaCl that was induced by intracranial injections of renin or angiotensin II. However, the increased water intake during the 18 h after the administration of renin was reduced to normal levels in adrenalectomized rats. Similar results were obtained with hypophysectomized rats. These results demonstrated that the delayed sodium appetite induced by renin or angiotensin II is not secondary to the stimulation of release of hormones from the pituitary gland or adrenal cortex.

WATER METABOLISM IN THE HYPOPHYSECTOMIZED BRATTLEBORO (DI) RAT

1969 ◽  
Vol 61 (4) ◽  
pp. 720-728 ◽  
Author(s):  
John W. Bauman ◽  
C. Van Wegen ◽  
J. Weil-Malherbe
Keyword(s):  
Diabetes Insipidus ◽  
Water Intake ◽  
Hormone Replacement ◽  
Pituitary Hormones ◽  
Water Metabolism ◽  
Similar Treatment ◽  
Pituitary Glands ◽  
Hereditary Diabetes ◽  
Hereditary Diabetes Insipidus ◽  
Reduced Water

ABSTRACT To re-examine the relative roles of the anterior and posterior pituitary hormones in diabetes insipidus, the effects of hypophysectomy and hormone replacement therapy in hereditary diabetes insipidus rats (Brattleboro strain) was compared with effect of similar treatment of rats without diabetes insipidus. In agreement with experiments on surgically induced diabetes insipidus, hypophysectomy sharply reduced water intake in rats with hereditary diabetes insipidus (DI rats). Water intake remained considerably higher, however, in these rats than in the non-DI rats following hypophysectomy. ADH treatment reduced water intake nearly to levels seen in non-DI rats. In water deprivation studies it was found that urine concentrating ability of the hypophysectomized non-DI rats was almost twice that of the hypophysectomized DI rats. None of the hormones tested restored water turnover of the hypophysectomized DI rats to that seen in sham operated controls. ACTH and T3 increased water intake, but not to levels seen in DI rats with intact pituitary glands. These experiments lead us to concur with those who hold that maximal flow in diabetes insipidus requires the participation of the anterior pituitary hormones. In addition these experiments indicate that ADH or ADH like material is physiologically functional in hypophysectomized rats (other than the Brattleboro strain), and that its presence accounts for the absence of diabetes insipidus following pituitary removal.

Food and water intake following lesions or electrical stimulation of the amygdala

1963 ◽  
Vol 205 (4) ◽  
pp. 761-765 ◽  
Author(s):  
Sebastian P. Grossman ◽  
Lore Grossman
Keyword(s):  
Electrical Stimulation ◽  
Food Intake ◽  
Water Intake ◽  
Water Consumption ◽  
Drinking Behavior ◽  
Food And Water Intake ◽  
Bilateral Lesions ◽  
Reduced Water ◽  
Observation Period ◽  
Stimulation Of

In the first experiment, very small bilateral lesions were placed into the posteroventral amygdala of 12 rats. Food and water intake was recorded for 6 weeks prior to the operation and for 12 weeks following it. Water consumption rose sharply immediately after the operation and remained near the maximal level for 12–16 days. Food intake increased gradually, reaching a maximum after 3–4 weeks. Feeding and drinking returned to near-normal within the 12-week observation period. In the second experiment, electrodes were implanted into anterior, medial, and posterior portions of the ventral amygdala. Electrical stimulation of anterior points inhibited food intake but increased water consumption. Stimulation of the medial placements produced no consistent effect. Both feeding and drinking behavior were inhibited during and immediately following the stimulation of posterior points. Lesions in the anterior area increased food intake but reduced water consumption. Medial lesions reduced water intake but had no reliable effect on feeding behavior. Posterior lesions produced hyperphagia and hyperdipsia. The lesion effects appeared to be permanent.

Stimulation of the conversion of corticosterone to aldosterone by sodium and water depletion of potassium-deficient rats. Comparison of different experimental procedures

1981 ◽  
Vol 96 (4) ◽  
pp. 519-526 ◽  
Author(s):  
Philippe Haldy ◽  
Jürg Müller
Keyword(s):  
Polyethylene Glycol ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Water Restriction ◽  
Deficient Diet ◽  
Water Depletion ◽  
Sodium And Potassium ◽  
Stimulation Of

Abstract. Sodium depletion, hypovolaemia or both were induced in potassium-depleted rats by various experimental protocols in order to study mechanisms involved in the regulation of late steps in aldosterone biosynthesis. The relative effects of such manoeuvres upon aldosterone biosynthesis and upon the plasma renin activity were compared. The conversion of corticosterone to aldosterone by incubated adrenal glands could be stimulated by a factor of 3 to 4 within 48 h by each of the following procedures: feeding on a sodium- and potassium-deficient diet or on sucrose, water restriction or treatment with furosemide. A 20-fold stimulation was elicited by experimental oedema due to subcutaneous polyethylene glycol solution or formalin. Intermediate responses were obtained by combining the sodium- and potassium-deficient diet with either water restriction or furosemide treatment as well as by the infusion of angiotensin II. Significant increases in the plasma renin activity, which were however not proportional to the stimulation of aldosterone biosynthesis, were seen in rats kept on the sodium- and potassium-deficient diet or treated by furosemide, polyethylene glycol or formalin, but not in rats kept on sucrose or deprived of water. An elevation in the plasma potassium concentration was observed only in the animals treated with water restriction. These results indicate that during potassium deficiency the stimulation of late steps in aldosterone biosynthesis by sodium and water depletion is mediated by the renin-angiotensin system and by an unknown mechanism which enhances the sensitivity of the zona glomerulosa to angiotensin II. Experimental oedema in potassium-deficient rats seems to be a useful model for further investigations of this mechanism.

Direct adrenergic and cholinergic stimulation of hypothalamic mechanisms

1962 ◽  
Vol 202 (5) ◽  
pp. 872-882 ◽  
Author(s):  
S. P. Grossman
Keyword(s):  
Food Intake ◽  
Water Intake ◽  
Albino Rats ◽  
Cholinergic Stimulation ◽  
Adrenergic Stimulation ◽  
Acid Base ◽  
Osmotic Stimulation ◽  
Mammillothalamic Tract ◽  
Histological Verification ◽  
Stimulation Of

Double-walled cannulas, allowing repeated stimulation of the same site in unrestrained animals with crystalline chemicals, were implanted stereotaxically into the hypothalamus of 36 albino rats. Histological verification of the intended placements showed that the tips of the cannulas were located in an area between the fornix and the mammillothalamic tract, lateral and dorsal to the ventromedial nuclei. Placement of minute amounts of adrenergic substances (epinephrine and norepinephrine) into this area induced vigorous and prolonged eating in satiated animals. Placement of comparable quantities of cholinergic substances (acetylcholine and carbachol) into identical loci in the same animals induced vigorous and prolonged drinking in satiated rats. Adrenergic stimulation increased the food intake of normally hungry animals but decreased the water intake of normally thirsty rats. Similarly, cholinergic stimulation increased the water intake of normally thirsty animals but decreased the food intake of normally hungry animals. Control tests indicated that such side effects of norepinephrine and carbachol as nonspecific activation, osmotic stimulation, vasomotor effects, and changes in the local acid-base composition can be ruled out as potential explanations of the observed results.

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