scholarly journals Angiotensin II-induced drinking behavior as a method to verify cannula placement into the cerebral ventricles of mice: An evaluation of its accuracy

2021 ◽  
Vol 232 ◽  
pp. 113339
Author(s):  
Nadine Faesel ◽  
Maik Schünemann ◽  
Michael Koch ◽  
Markus Fendt
Keyword(s):  
Angiotensin Ii ◽  
Drinking Behavior ◽  
Cerebral Ventricles ◽  
Cannula Placement

Effect of intravenous angiotensin II on Fos distribution and drinking behavior in rabbits

1997 ◽  
Vol 272 (5) ◽  
pp. R1515-R1524 ◽  
Author(s):  
E. Badoer ◽  
D. McKinlay
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Intravenous Infusion ◽  
Drinking Behavior ◽  
Ventrolateral Medulla ◽  
Lamina Terminalis ◽  
Ang Ii ◽  
Solitary Tract ◽  
Cell Nuclei ◽  
Drinking Response

We investigated the effect of intravenous infusion of angiotensin II (ANG II, 40 ng.kg-1.min-1) on the distribution of Fos in the subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT), and the medulla of the conscious rabbit. ANG II elicited significant increases in the number of Fos-positive cell nuclei in the SFO and OVLT (15- and 10-fold, respectively). Raising blood pressure with phenylephrine did not elicit Fos in these nuclei. These nuclei are believed to be responsible for the dipsogenic actions of ANG II; however, ANG II was not dipsogenic. When blood pressure was held at preinfusion levels by the coadministration of sodium nitroprus-side and ANG II, the rabbits did not drink but Fos production in the lamina terminalis was elevated. In the medulla, ANG II did not significantly increase Fos production in the nucleus of the solitary tract (NTS) or ventrolateral medulla (VLM). However, with the coadministration of sodium nitroprusside, there were marked increases in the NTS and VLM. The results suggest that neurons in the SFO and OVLT are either not involved in the dipsogenic pathways or there is disruption further downstream in the central pathways that would normally mediate a drinking response to ANG II.

Subfornical organ: forebrain site of pressor and dipsogenic action of angiotensin II

1980 ◽  
Vol 239 (5) ◽  
pp. R382-R389 ◽  
Author(s):  
M. L. Mangiapane ◽  
J. B. Simpson
Keyword(s):  
Angiotensin Ii ◽  
Drinking Behavior ◽  
Subfornical Organ ◽  
Pressor Effect ◽  
Intracranial Injection ◽  
Physiological Range ◽  
A Site ◽  
Alternative Sites

Intracranial injection of angiotensin II (AII) at three brain sites elicited near simultaneous dipsogenic and pressor effects in rats. Both effects were maximal, occurred with the shortest latencies, and at the lowest doses of AII when the cannula terminated precisely within the parenchyma of the subfornical organ (SFO). Pressor effects were produced by SFO injection of a dose of AII (0.1 pg) which approximates plasma AII concentrations at the high end of the physiological range. Both the drinking and pressor effects were blocked by saralasin. Injections of AII at sites immediately adjacent to SFO produced smaller effects with longer latencies. These results ruled out the possibility that SFO injections were effective via leakage to alternative sites. The pressor effect of AII at the SFO remained in animals under chloralose anesthesia, demonstrating that it is not an artifact of drinking behavior. These results indicate that the SFO is a site of AII pressor action, and confirm previous demonstrations that the structure is a site of AII drinking action.

Effect of Intraventricular Perfusion of Angiotensin II in Conscious Normal Rats and in Rats with Hereditary Hypothalamic Diabetes Insipidus

1976 ◽  
Vol 51 (s3) ◽  
pp. 391s-394s
Author(s):  
J. S. Hutchinson ◽  
P. Schelling ◽  
J. Möhring ◽  
D. Ganten
Keyword(s):  
Angiotensin Ii ◽  
Diabetes Insipidus ◽  
Pressor Response ◽  
Cerebral Ventricles ◽  
Basal Secretion ◽  
Artificial Cerebrospinal Fluid ◽  
Pressor Responses ◽  
Long Evans ◽  
Hereditary Hypothalamic Diabetes Insipidus ◽  
Intact Rats

1. Artificial cerebrospinal fluid was perfused through the cerebral ventricles of conscious rats. A basal secretion rate of 16 ± 3 × 10—15 mol of immunoreactive angiotensin 11/min was calculated for intact rats. 2. Most of the immunoreactive angiotensin II consisted probably of the heptapeptide or pentapeptide angiotensin II fragments. 3. The pressor responses to intraventricular perfusions of angiotensin II were normal in Long—Evans rats, virtually absent in rats homozygous for hereditary hypothalamic diabetes insipidus, irrespective of whether they were injected with vasopressin tannate or not, and intermediate in rats heterozygous for hypothalamic diabetes insipidus. 4. The results suggest that the pressor response to intraventricular angiotensin II is related to the release of vasopressin.

Effects of peptide and non-peptide antagonists of angiotensin II receptors on drinking behavior in rats

1999 ◽  
Vol 93 (3) ◽  
pp. 219-224 ◽  
Author(s):  
L.G. Alova ◽  
S.L. Stancheva ◽  
J. Matsoukas ◽  
V.P. Georgiev
Keyword(s):  
Angiotensin Ii ◽  
Drinking Behavior ◽  
Angiotensin Ii Receptors

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.

Endogenous renin-angiotensin system and drinking behavior in flounder

1985 ◽  
Vol 248 (2) ◽  
pp. R157-R160 ◽  
Author(s):  
R. J. Balment ◽  
S. Carrick
Keyword(s):  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Drinking Behavior ◽  
Renin Angiotensin System ◽  
Simultaneous Administration ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Physiological Importance ◽  
Plasma Chloride

High rates of drinking in seawater-adapted, compared with freshwater (FW)-adapted, flounder were associated with raised plasma chloride and osmotic concentrations. Hypotension in FW-adapted fish, after papaverine administration, gave rise to greatly elevated rates of drinking. This dipsogenic response apparently relied on activation of the endogenous renin-angiotensin system (RAS) and was abolished by simultaneous administration of the converting enzyme inhibitor, captopril. Exogenous angiotensin II was shown to be dipsogenic and vasopressor in the FW-adapted fish. The physiological importance of the activation of the RAS in the control of drinking behavior in euryhaline fish is discussed.

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.

Circulating angiotensin II and drinking behavior in rats

1990 ◽  
Vol 259 (3) ◽  
pp. R531-R538 ◽  
Author(s):  
C. M. Pawloski ◽  
G. D. Fink
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Dose Range ◽  
Drinking Behavior ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Physiological Conditions ◽  
Water Drinking ◽  
Sprague Dawley Rats ◽  
Before And After

This study was designed to investigate the effects on water drinking of acute and chronic increases in circulating angiotensin II (ANG II) concentrations in rats. Experiments were conducted in male Sprague-Dawley rats chronically instrumented with femoral arterial and venous catheters and permanently housed in metal metabolism cages. ANG II was infused intravenously either acutely (30 min-2 h) or chronically (3 days) in a dose range of 10-60 ng/min. In no instance did such infusions cause a statistically significant increase in water intake. Other experiments examined the influence of ANG II (10 ng/min iv) on drinking elicited by infusion of hypertonic sodium chloride (1.5 M at 3.5 microliters/min). ANG II administration did not increase drinking to a hypertonic saline stimulus or lower the osmotic threshold for drinking. Nitroprusside (12 micrograms/min) was infused for 30 min to produce hypotension and drinking. Water intake associated with this stimulus was not changed by blocking ANG II formation with enalapril (2 mg/kg iv) or by concomitant infusion of ANG II (10 ng/min iv). Finally, plasma ANG II concentrations were measured before and after 1-h intravenous infusion of saline or ANG II to determine the levels of circulating ANG II produced by the infusion rates used here. It is concluded that the range of circulating ANG II concentrations found under most physiological conditions in rats does not directly stimulate drinking or participate importantly in osmotic or hypotension-induced drinking.

Nitric oxide modulates angiotensin II–induced drinking behavior in the near-term ovine fetus

2000 ◽  
Vol 182 (3) ◽  
pp. 713-719 ◽  
Author(s):  
Mostafa A. El-Haddad ◽  
Conrad R. Chao ◽  
Sheng-xing Ma ◽  
Michael G. Ross
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Drinking Behavior ◽  
Ovine Fetus ◽  
Near Term
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