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.

scholarly journals mTORC1 Signaling Contributes to Drinking But Not Blood Pressure Responses to Brain Angiotensin II

Endocrinology ◽  
2016 ◽  
Vol 157 (8) ◽  
pp. 3140-3148 ◽  
Author(s):  
Kenjiro Muta ◽  
Donald A. Morgan ◽  
Justin L. Grobe ◽  
Curt D. Sigmund ◽  
Kamal Rahmouni
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Drinking Behavior ◽  
Subfornical Organ ◽  
Dependent Manner ◽  
Ang Ii ◽  
Mtorc1 Signaling ◽  
Wide Range ◽  
The Brain

Mechanistic target of rapamycin complex 1 (mTORC1) is a molecular node that couples extracellular cues to a wide range of cellular events controlling various physiological processes. Here, we identified mTORC1 signaling as a critical mediator of angiotensin II (Ang II) action in the brain. In neuronal GT1–7 cells, we show that Ang II stimulates neuronal mTORC1 signaling in an Ang II type 1 receptor-dependent manner. In mice, a single intracerebroventricular (ICV) injection or chronic sc infusion of Ang II activated mTORC1 signaling in the subfornical organ, a critical brain region in cardiovascular control and fluid balance. Moreover, transgenic sRA mice with brain-specific overproduction of Ang II displayed increased mTORC1 signaling in the subfornical organ. To test the functional role of brain mTORC1 in mediating the action of Ang II, we examined the consequence of mTORC1 inhibition with rapamycin on Ang II-induced increase in water intake and arterial pressure. ICV pretreatment with rapamycin blocked ICV Ang II-mediated increases in the frequency, duration, and amount of water intake but did not interfere with the pressor response evoked by Ang II. In addition, ICV delivery of rapamycin significantly reduced polydipsia, but not hypertension, of sRA mice. These results demonstrate that mTORC1 is a novel downstream pathway of Ang II type 1 receptor signaling in the brain and selectively mediates the effect of Ang II on drinking behavior.

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.

Effect of Ablation of the Subfornical Organ on Water Intake Elicited by Systemically Administered Angiotensin-II

1974 ◽  
Vol 52 (6) ◽  
pp. 1217-1220 ◽  
Author(s):  
A. E. Abdelaal ◽  
S. Y. Assaf ◽  
J. Kucharczyk ◽  
G. J. Mogenson
Keyword(s):  
Angiotensin Ii ◽  
Continuous Infusion ◽  
Water Intake ◽  
Receptor Site ◽  
Subfornical Organ ◽  
Electrolytic Lesions

The effect of electrolytic lesions of the subfornical organ on water intake induced by the continuous infusion of angiotensin-II through a chronic jugular cannula was studied. Lesions of the subfornical organ significantly reduced but did not abolish the elicited drinking. These results support the hypothesis that the subfornical organ is a receptor site for angiotensin-II but also suggest that this may not be the only site of receptors.

scholarly journals Circumventricular organs and ANG II-induced salt appetite: blood pressure and connectivity

2000 ◽  
Vol 279 (6) ◽  
pp. R2277-R2286 ◽  
Author(s):  
Douglas A. Fitts ◽  
Elizabeth M. Starbuck ◽  
Alexandra Ruhf
Keyword(s):  
Blood Pressure ◽  
Water Intake ◽  
Femoral Vein ◽  
Circumventricular Organs ◽  
Subfornical Organ ◽  
Salt Appetite ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Apparent Contradiction ◽  
Organum Vasculosum Laminae Terminalis

A lesion of the subfornical organ (SFO) may reduce sodium depletion-induced salt appetite, which is largely dependent on ANG II, and yet ANG II infusions directly into SFO do not provoke salt appetite. Two experiments were designed to address this apparent contradiction. In experiment 1 sustained infusions of ANG II into SFO did not produce a sustained elevation of blood pressure, and neither a reduction of blood pressure alone with minoxidil and captopril nor a reduction of both blood pressure and volume with furosemide and captopril enhanced salt appetite. Infusions of ANG II in the organum vasculosum laminae terminalis (OVLT) did evoke salt appetite without raising blood pressure. In experiment 2 knife cuts of the afferent and efferent fibers of the rostroventral pole of the SFO abolished water intake during an infusion of ANG II into the femoral vein but failed to reduce salt appetite during an infusion of ANG II into the OVLT. We conclude that 1) hypertension does not account for the failure of infusions of ANG II in the SFO to generate salt appetite and 2) the OVLT does not depend on its connectivity with the SFO to generate salt appetite during ANG II infusions.

Cerebral metabolic and hormonal activations during hemorrhage in sinoaortic-denervated rats

1990 ◽  
Vol 259 (2) ◽  
pp. R305-R312 ◽  
Author(s):  
M. Kadekaro ◽  
J. Y. Summy-Long ◽  
M. L. Terrell ◽  
H. Lekan ◽  
H. E. Gary ◽  
...  
Keyword(s):  
High Pressure ◽  
Angiotensin Ii ◽  
Glucose Metabolism ◽  
Blood Volume ◽  
Glucose Utilization ◽  
Area Postrema ◽  
Subfornical Organ ◽  
Neural Lobe ◽  
Metabolic Activities ◽  
Supraoptic Nuclei

Denervation of sinoaortic baroreceptors in normovolemic rats selectively increases glucose utilization in the median eminence and pituitary neural lobe and enhances secretion of vasopressin and oxytocin. Hemorrhage in denervated animals increases further glucose metabolism in these structures and stimulates the release of both neurohypophysial hormones with preferentially a greater effect on vasopressin. Similar increases in glucose metabolism in these structures with a greater release of vasopressin are observed in sham-operated animals during hemorrhage. Absence of high-pressure receptors, therefore, does not modify the preferential release of vasopressin during hypovolemia. Hemorrhage also increases glucose utilization in the paraventricular and supraoptic nuclei, area postrema, and subfornical organ in sham-operated and denervated rats but only after a 20% blood reduction. The results indicate that decreased inputs from low-pressure receptors during hemorrhage increase the activity of the hypothalamoneurohypophysial system after small reductions in blood volume and that the activity of this system is tonically inhibited by baroreceptors. The activities of structures responsive to circulating angiotensin II (subfornical organ and area postrema) are stimulated by larger reductions in blood volume and their metabolic activities are not tonically influenced by high-pressure receptors.

Salt appetite in rat pups: ontogeny of angiotensin II-aldosterone synergy

1991 ◽  
Vol 260 (2) ◽  
pp. R421-R429 ◽  
Author(s):  
C. I. Thompson ◽  
A. N. Epstein
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Salt Intake ◽  
Neural Mechanisms ◽  
Salt Appetite ◽  
Ang Ii ◽  
Rat Pups ◽  
Effective Doses ◽  
Old Rats ◽  
Individual Actions

Preweanling rats were tested to determine whether angiotensin II (ANG II) and aldosterone (Aldo) act synergistically to enhance salt appetite at 12 and 17 days. Twelve-day-old pups received one of four hormone treatments in four doses: 1) ANG II only [1, 2, 10, or 100 ng pulse intracerebroventricular (icv)], 2) Aldo only (1, 2, 10, or 40 micrograms/day sc), 3) Aldo + ANG II (four individual doses combined), or 4) vehicle. Seventeen-day-old rats received the same treatments in two doses (2 or 100 ng ANG II; 2 or 40 micrograms Aldo). Pups were presatiated with milk through anterior oral catheters and then given either 4% NaCl or water for 30 min. Intake was assessed by body weight change. At both ages, ANG II enhanced salt (and water) intake, and Aldo enhanced salt (but not water) intake. Minimum effective doses were comparable to those reported for adults. ANG II-Aldo synergy was absent at 12 days and present at 17 days, when salt intake was 590% greater than the summed intakes evoked by ANG II and Aldo alone. The neural mechanisms for ANG II-Aldo synergy thus mature later than those mediating the hormone's individual actions in arousing salt appetite.

Involvement of angiotensin II in water intake of genetically polydipsic mice

1991 ◽  
Vol 260 (6) ◽  
pp. R1152-R1158 ◽  
Author(s):  
T. Katafuchi ◽  
Y. Hattori ◽  
I. Nagatomo ◽  
K. Koizumi ◽  
E. Silverstein
Keyword(s):  
Angiotensin Ii ◽  
Food Intake ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Dark Period ◽  
Plasma Renin ◽  
Ang Ii ◽  
Arterial Blood ◽  
Daily Water Intake ◽  
Reduced Drinking

The involvement of angiotensin II (ANG II) in the genetic polydipsia of the STR/N strain of mice was investigated. Daily water intake of the polydipsic inbred STR/N of both sexes ranged between five and eight times that of nonpolydipsic controls: STR/1N, a mutant of the STR/N, and Swiss-Webster (S/W) mice. Nevertheless the diurnal pattern of drinking was maintained in the STR/N. There was no difference in daily food intake, arterial blood pressure, and plasma renin activity among the three groups. Drinking responses to 48 h of water deprivation were not significantly different between the polydipsic mice and their control groups. Captopril, an angiotensin I converting-enzyme inhibitor, injected subcutaneously just before the dark period, reduced drinking for 6 h in the polydipsic strain only. Food intake of all three groups of mice was not affected. Similarly the ANG II antagonist saralasin, [Sar1,-Ile8]ANG II, injected into the lateral cerebroventricle just before the dark period, significantly reduced water intake for 6 h after injection in the polydipsic mice only. Intracerebroventricular injection of ANG II increased drinking in the nondeprived controls but not in the polydipsic mice. These findings suggest that the polydipsia in the STR/N mice may involve, at least in part, the ANG II system in the brain.

Angiotensin and salt appetite of BALB/c mice

1990 ◽  
Vol 259 (4) ◽  
pp. R729-R735 ◽  
Author(s):  
D. A. Denton ◽  
J. R. Blair-West ◽  
M. McBurnie ◽  
P. G. Osborne ◽  
E. Tarjan ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sodium Content ◽  
Neural Systems ◽  
Salt Appetite ◽  
Nacl Solution ◽  
Sodium Appetite ◽  
Daily Water Intake ◽  
Body Sodium ◽  
Daily Water ◽  
Ingestive Behaviors

The influence of systemic or intracerebroventricular (icv) administration of angiotensin II on the intakes of NaCl solution, water, and food was investigated in BALB/c mice. Systemic administration of angiotensin II had little, if any, influence on these ingestive behaviors. On the other hand, icv infusion of angiotensin II at 70 ng/day increased (P less than 0.05) intakes of NaCl solution and water by the third day of infusion. The amount of NaCl ingested daily during the infusion was two to three times body sodium content. The mean daily water intake increased to 40-60% of body weight. The vast increase in NaCl intake was not secondary to a natriuresis caused by the icv infusion of angiotensin II. The results suggest that angiotensin II has a direct effect on neural systems involved in sodium appetite in this species.

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