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.

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.

Water intake elicited by injections of angiotensin II into preoptic area of rats

1981 ◽  
Vol 240 (1) ◽  
pp. R70-R74 ◽  
Author(s):  
D. B. Richardson ◽  
G. J. Mogenson
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Preoptic Area ◽  
High Dose ◽  
Preoptic Nucleus ◽  
Cerebral Ventricles ◽  
Preoptic Region ◽  
Medial Preoptic Nucleus ◽  
Autoradiographic Analysis

Drinking in response to unilateral injections of angiotensin II (AII) into the preoptic area is relatively weak and a relatively high dose of AII is required. A comparison was made of the drinking elicited by bilateral and unilateral injections of AII. Reliable drinking was observed when 5 X 10(-12) mol of AII in 0.2 microliter was injected bilaterally into the preoptic area, and in some animals when the dose of AII was 0.5 X 10(-12) mol in 0.2 microliter. The volumes of water intake were significantly larger with bilateral injections compared to unilateral injections. By injection of tritiated AII to elicit drinking and subsequent autoradiographic analysis of brain sections, it was shown that the injections were confined to the preoptic region and did not reach the cerebral ventricles. The results suggest that 1) bilateral injections may be more appropriate for comparing the preoptic region with other putative angiotensin receptive sites, 2) there is a greater responsiveness of the preoptic region to bilateral as compared with unilateral injections, and 3) the AII receptive area is diffusely represented in the region of the medial preoptic nucleus.

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.

Role of brain angiotensin II in thirst and sodium appetite of sheep

1997 ◽  
Vol 273 (1) ◽  
pp. R187-R196 ◽  
Author(s):  
R. S. Weisinger ◽  
J. R. Blair-West ◽  
D. A. Denton ◽  
E. Tarjan
Keyword(s):  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Water Intake ◽  
Neural System ◽  
At1 Receptor ◽  
Hypertonic Solution ◽  
Ang Ii ◽  
Sodium Appetite ◽  
Intracerebroventricular Infusion

The contribution of brain angiotensin II (ANG II) to thirst and Na+ appetite of sheep was evaluated. Thirst was stimulated by water deprivation, intracarotid or intracerebroventricular infusion of ANG II, or intracarotid or intracerebroventricular infusion of hypertonic solution. Intracerebroventricular infusion, over 1-3 h, of the ANG II type 1 (AT1) receptor antagonist, losartan, decreased or abolished water intake caused by all of the stimuli tested. Intracerebroventricular infusion of ZD-7155, another AT1-receptor antagonist, blocked ANG II-induced water intake. Neither losartan nor ZD-7155 infused intracerebroventricularly altered the Na+ appetite of Na(+)-depleted sheep. Intracerebroventricular infusion of losartan over 3 h, however, did block the increase in water intake and the decrease in Na+ intake caused by intracerebroventricular infusion of hypertonic NaCl in Na(+)-depleted sheep. Intracerebroventricular infusion of the ANG II type 2 (AT2) receptor antagonist, PD-123319, over 1-3 h, did not alter ANG II-induced water intake or Na+ depletion-induced Na+ intake. These results are consistent with the proposition that brain ANG II, working via AT1 receptors, is involved in the neural system controlling some aspects of physiological thirst and Na+ appetite. A role for AT2 receptors in physiological thirst or Na+ appetite is not supported by the present results.

Angiotensin-related sodium appetite and thirst in cattle

1988 ◽  
Vol 255 (2) ◽  
pp. R205-R211 ◽  
Author(s):  
J. R. Blair-West ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
R. S. Weisinger
Keyword(s):  
Angiotensin Ii ◽  
Blood Brain Barrier ◽  
Water Intake ◽  
Lateral Ventricle ◽  
Circumventricular Organs ◽  
Brain Barrier ◽  
Angiotensin Ii Receptors ◽  
Nacl Solution ◽  
Sodium Appetite ◽  
The Brain

Cows depleted of Na by loss of saliva from a parotid fistula for 46 h had an avid appetite for Na solution. They drank 21.0 +/- 1.6 liter of 0.3 M NaHCO3-NaCl solution during 2 h of access but little or no water during that time. Solutions of angiotensin II or captopril were infused for 3 h intravenously or into a lateral ventricle (intracerebroventricular) beginning 1 h before access to Na solution. Intravenous angiotensin II increased Na intake (to 26.8 +/- 2.9 liter, P less than 0.01) but did not alter water intake. Intracerebroventricular angiotensin II increased water intake but did not alter Na intake. Intravenous captopril reduced Na intake (to 11.0 +/- 2.1 liter, P less than 0.001) and concurrent intravenous angiotensin II prevented the reduction but concurrent intracerebroventricular angiotensin II did not. Intracerebroventricular captopril did not alter Na or water intake. Intravenous captopril reduced to zero the water intake during the hour before Na access, and concurrent intravenous angiotensin II prevented that reduction also. The dipsogenic action of intracerebroventricular angiotensin II was potentiated by intravenous captopril. The results of these experiments suggest that if angiotensin II receptors involved in the mechanism regulating Na appetite are in the brain, they are accessible only from the blood, e.g., in circumventricular organs. Thirst was inhibited by reduction of angiotensin II in blood but was stimulated only by angiotensin II acting inside the blood-brain barrier.

Sodium appetite and thirst in cattle subjected to dehydration

1989 ◽  
Vol 257 (5) ◽  
pp. R1212-R1218 ◽  
Author(s):  
J. R. Blair-West ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
R. S. Weisinger
Keyword(s):  
Angiotensin Ii ◽  
Extracellular Fluid ◽  
Extracellular Fluid Volume ◽  
Angiotensin Ii Receptors ◽  
Free Access ◽  
Nacl Solution ◽  
Sodium Appetite ◽  
Site Of Action ◽  
Access To Water ◽  
The Brain

Cows having free access to water (hydrated) or deprived of water for 26.5 h (dehydrated) were infused for 3 h with angiotensin II or captopril solutions intravenously (iv) or intracerebroventricularly (icv) beginning 1 h before access to 0.3 M NaHCO3/NaCl solution for 2 h. The results agree with the results of the experiments with the same agents and doses in Na-deficient cows. Only iv infusion of angiotensin II stimulated Na appetite and only icv infusion of angiotensin II stimulated thirst. Therefore, barriers to the penetration of angiotensin II in the brain determined the particular site of action and elicited response. Dehydration did not stimulate Na appetite and, as shown previously, Na deficiency did not stimulate thirst, but both behaviors seem to be influenced by angiotensin-related mechanisms in the brain. The inability of iv angiotensin II to stimulate Na appetite in hydrated cows might be explained by the lack of a response caused by, and common to, Na deficiency and dehydration, e.g., upregulation of angiotensin II receptors, or reduced extracellular fluid volume.

Activator protein-1 is necessary for angiotensin-II stimulation of human adrenocorticotropin receptor gene transcription

2001 ◽  
Vol 268 (6) ◽  
pp. 1802-1810
Author(s):  
Danielle Naville ◽  
Estelle Bordet ◽  
Marie-Claude Berthelon ◽  
Philippe Durand ◽  
Martine Begeot
Keyword(s):  
Angiotensin Ii ◽  
Gene Transcription ◽  
Receptor Gene ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
Stimulation Of

scholarly journals Stimulation of 1,2-diacylglycerol accumulation in hepatocytes by vasopressin, epinephrine, and angiotensin II.

1985 ◽  
Vol 260 (26) ◽  
pp. 14201-14207 ◽  
Author(s):  
S B Bocckino ◽  
P F Blackmore ◽  
J H Exton
Keyword(s):  
Angiotensin Ii ◽  
Stimulation Of
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