Enhanced central response to dehydration in mice lacking angiotensin AT1a receptors

2001 ◽  
Vol 280 (4) ◽  
pp. R1177-R1184 ◽  
Author(s):  
Mariana Morris ◽  
Shelia Means ◽  
Michael I. Oliverio ◽  
Thomas M. Coffman
Keyword(s):  
Central Nervous System ◽  
Water Deprivation ◽  
Plasma Osmolality ◽  
Mrna Levels ◽  
Posterior Pituitary ◽  
High Data ◽  
Plasma Vasopressin ◽  
Fos Protein ◽  
Central Response ◽  
The Central Nervous System

The objective was to determine the central nervous system (CNS) responses to dehydration (c-Fos and vasopressin mRNA) in mice lacking the ANG AT1a receptor [ANG AT1a knockout (KO)]. Control and AT1a KO mice were dehydrated for 24 or 48 h. Baseline plasma vasopressin (VP) was not different between the groups; however, the response to dehydration was attenuated in AT1a KO (24 ± 11 vs. 10.6 ± 2.7 pg/ml). Dehydration produced similar increases in plasma osmolality and depletion of posterior pituitary VP content. Neuronal activation was observed as increases in c-Fos protein and VP mRNA. The supraoptic responses were not different between groups. In the paraventricular nucleus (PVN), c-Fos-positive neurons (57.4 ± 10.7 vs. 98.4 ± 7.4 c-Fos cells/PVN, control vs. AT1aKO) and VP mRNA levels (1.0 ± 0.1 vs. 1.4 ± 0.1 μCi, control vs. AT1a KO) were increased with greater responses in AT1a KO. A comparison of 1- to 2-day water deprivation showed that plasma VP, brain c-Fos, and VP mRNA returned toward control on day 2, although plasma osmolality remained high. Data demonstrate that AT1a KO mice show a dichotomous response to dehydration, reduced for plasma VP and enhanced for PVN c-Fos protein and VP mRNA. The results illustrate the importance of ANG AT1a receptors in the regulation of osmotic and endocrine balance.

Effects of water deprivation on immunoreactive angiotensin II levels in plasma, cerebroventricular perfusate and hypothalamus of the rat

1981 ◽  
Vol 97 (1) ◽  
pp. 137-144 ◽  
Author(s):  
K. Yamaguchi
Keyword(s):  
Central Nervous System ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Water Deprivation ◽  
Potassium Concentration ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Anaesthetized Rats ◽  
The Central Nervous System ◽  
The Brain

Abstract. To examine whether endogenous angiotensin — which has been suggested to produce increased vasopressin (ADH) release and water intake under dehydration, by stimulating the central nervous system — is derived from the brain or from the circulating blood or from both, the effects of water deprivation for 46 h on immunoreactive angiotensin II (AII) concentrations of plasma, cerebroventricular perfusate and the hypothalamus were studied in conscious and urethane-anaesthetized rats. Immunoreactive AII in plasma and the hypothalamus was extracted with acetone and petroleum ether preceding the determination by radioimmunoassay. The water deprivation significantly increased plasma immunoreactive AII concentration (P < 0.002) together with plasma osmolality and sodium concentration, and reduced the potassium concentration. However, neither the immunoreactive AII concentration of the ventricular perfusate nor that of the hypothalamus was affected. Both the perfusate and the hypothalamus were very poor in immunoreactive AII (< 35.0 pg/ml and < 46.7 pg/g wet tissue, respectively). These results may suggest that increased ADH release and water intake under dehydration are brought about by the angiotensin formed in the circulating blood rather than in the brain.

Suppressed basal antidiuretic hormone release during cyclooxygenase inhibition in conscious dogs

1983 ◽  
Vol 244 (4) ◽  
pp. R487-R491
Author(s):  
B. R. Walker
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Antidiuretic Hormone ◽  
Plasma Osmolality ◽  
Blood Gases ◽  
Conscious Dogs ◽  
Arterial Blood ◽  
The Central Nervous System

Both in vitro and in vivo experiments suggest that prostaglandins may affect antidiuretic hormone (ADH) release centrally. In addition, other studies show that prostaglandins administered peripherally may cause ADH release. However, these latter studies have been flawed by hemodynamic alterations and the use of anesthetics, which make interpretation difficult. The present study was designed to test for involvement of prostaglandins produced outside the central nervous system in ADH release in conscious dogs. Administration of meclofenamate (2 mg/kg and 2 mg X kg-1 X h 1, iv) resulted in a consistent fall in plasma ADH levels in five dogs. This diminution of ADH release occurred with no change in systemic hemodynamics, arterial blood gases, or plasma osmolality, suggesting that prostaglandins are important mediators of basal ADH release in the conscious dog. Because meclofenamate does not cross the blood-brain barrier, prostaglandins produced outside the central nervous system appear to be involved in this process. The specific prostaglandin involved or the site of action of prostaglandins on ADH release is not clear at this time.

Inhibition of hypoxia-induced ADH release by meclofenamate in the conscious dog

1983 ◽  
Vol 54 (6) ◽  
pp. 1624-1629 ◽  
Author(s):  
B. R. Walker
Keyword(s):  
Central Nervous System ◽  
Plasma Osmolality ◽  
Hypoxic Exposure ◽  
Elevated Plasma ◽  
In Vivo Models ◽  
Conscious Dog ◽  
Prostaglandin Release ◽  
The Central Nervous System ◽  
Endogenous Prostaglandins

Release of antidiuretic hormone (ADH) due to hypoxic stimuli has been documented in several in vivo models. The current study was performed to determine whether 1) hypoxia causes ADH release in the conscious normovolemic dog and 2) whether endogenous prostaglandins are involved in hypoxic ADH release. Five conscious dogs were made hypoxic by inhalation of 10% O2. Dogs were studied both with and without pretreatment with meclofenamate (2 mg/kg iv and 2 mg . kg-1 . h-1). Hypoxic exposure resulted in elevated plasma ADH; however, meclofenamate totally blocked this response. Hemodynamic responses to hypoxia were unaffected by meclofenamate. In addition, plasma osmolality was unchanged by hypoxia in both groups. Since meclofenamate does not cross the blood-brain barrier, it is concluded that the release of ADH by hypoxia in the conscious dog may be mediated by endogenous prostaglandins produced outside the central nervous system. It appears that elevated renal prostaglandin release, increased ADH, and hemodynamic alterations could all interact to determine the final renal response to hypoxia.

Identifying c-fos Expression as a Strategy to Investigate the Actions of General Anesthetics on the Central Nervous System

2021 ◽  
Vol 19 ◽  
Author(s):  
Donghang Zhang ◽  
Jin Liu ◽  
Tao Zhu ◽  
Cheng Zhou
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Convenient Method ◽  
Early Gene ◽  
General Anesthetics ◽  
Physiological Conditions ◽  
Fos Protein ◽  
The Central Nervous System ◽  
Fos Expression ◽  
The Brain

: Although general anesthetics have been used in the clinic for more than 170 years, the ways in which they induce amnesia, unconsciousness, analgesia, and immobility remain elusive. Modulations of various neural nuclei and circuits are involved in the actions of general anesthetics. The expression of the immediate early gene c-fos and its nuclear product, c-fos protein can be induced by neuronal depolarization; therefore, c-fos staining is commonly used to identify the activated neurons during sleep and/or wakefulness, as well as in various physiological conditions in the central nervous system. Identifying c-fos expression is also a direct and convenient method to explore the effects of general anesthetics on the activity of neural nuclei and circuits. Using c-fos staining, general anesthetics have been found to interact with sleep- and wakefulness-promoting systems throughout the brain, which may explain their ability to induce unconsciousness and emergence from general anesthesia. This review summarizes the actions of general anesthetics on neural nuclei and circuits based on c-fos expression.

Divergent effects of intracerebroventricular and peripheral leptin administration on feeding and hypothalamic neuropeptide Y in lean and obese (fa/fa) Zucker rats

1999 ◽  
Vol 96 (3) ◽  
pp. 307-312 ◽  
Author(s):  
Simon DRYDEN ◽  
Peter KING ◽  
Lucy PICKAVANCE ◽  
Patrick DOYLE ◽  
Gareth WILLIAMS
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Leptin Receptor ◽  
Zucker Rats ◽  
Mrna Levels ◽  
Zucker Rat ◽  
Direct Effects ◽  
The Central Nervous System

Leptin inhibits feeding and decreases body weight. It may act partly by inhibiting hypothalamic neurons that express neuropeptide Y, a powerful inducer of feeding and obesity. These neuropeptide Y neurons express the Ob-Rb leptin receptor and are overactive in the fatty (fa/fa) Zucker rat. The fa mutation affects the extracellular domain of the leptin receptor, but its impact on leptin action and neuropeptide Y neuronal activity is not fully known. We compared the effects of three doses of leptin given intracerebroventricularly and three doses of leptin injected intraperitoneally on food intake and hypothalamic neuropeptide Y mRNA, in lean and fatty Zucker rats. In lean rats, 4-h food intake was reduced in a dose-related fashion (P< 0.01) by all intracerebroventricular leptin doses and by intraperitoneal doses of 300 and 600 μg/kg. Neuropeptide Y mRNA levels were reduced by 28% and 21% after the highest intracerebroventricular and intraperitoneal doses respectively (P< 0.01 for both). In fatty rats, only the highest intracerebroventricular leptin dose reduced food intake (by 22%; P< 0.01). Neuropeptide Y mRNA levels were 100% higher in fatty rats than in lean animals, and were reduced by 18% (P< 0.01) after the highest intracerebroventricular leptin dose. Intraperitoneal injection had no effect on food intake and neuropeptide Y mRNA. The fa/fa Zucker rat is therefore less sensitive to leptin given intracerebroventricularly and particularly intraperitoneally, suggesting that the fa mutation interferes both with leptin's direct effects on neurons and its transport into the central nervous system. Obesity in the fa/fa Zucker rat may be partly due to the inability of leptin to inhibit hypothalamic neuropeptide Y neurons.

Effects of intraventricular injection of Sar1-Ala8-angiotensin II on plasma vasopressin level increased by angiotensin II and by water deprivation in conscious rats

1980 ◽  
Vol 93 (4) ◽  
pp. 407-412 ◽  
Author(s):  
K. Yamaguchi ◽  
H. Hama ◽  
T. Sakaguchi ◽  
H. Negoro ◽  
K. Kamoi
Keyword(s):  
Angiotensin Ii ◽  
Water Deprivation ◽  
Plasma Osmolality ◽  
Male Rats ◽  
Intraventricular Injection ◽  
Plasma Vasopressin ◽  
Significant Difference ◽  
Median Plasma ◽  
Specific Antagonist ◽  
The Brain

Abstract. The effects of intraventricular injection of Sar1-Ala8-angiotensin II (a specific antagonist of angiotensin II) on the plasma vasopressin level increased by intraventricular injection of angiotensin II and by water deprivation (46 h) were examined in conscious male rats with an indwelling cannula in the third cerebral ventricle. Blood samplings were made by decapitation and the plasma level of vasopressin was determined by radioimmunoassay. Twenty-five, 50 or 100 ng of angiotensin II produced significant (P<0.05) increase in plasma vasopressin level 90 sec after the injection. The effect of 50 ng of angiotensin II was inhibited significantly (P<0.05) at least with 100 ng of Sar1-Ala8-angiotensin II given 2 min before the injection of angiotensin II. The dehydrated rats to which 1000 ng of Sar1-Ala8-angiotensin II was given 5 min before the decapitation showed the significantly (P<0.05) lower median plasma vasopressin level than that of the dehydrated controls. No significant difference in plasma osmolality was noted between them. These results suggest that the plasma vasopressin response to intraventricular angiotensin II is produced via angiotensin II receptors in the brain and that Sar1-Ala8-angiotensin II inhibits the effect of endogenous angiotensin II on plasma vasopressin level under dehydration.

scholarly journals Effects of ACTH, dexamethasone, and adrenalectomy on 11β-hydroxylase (CYP11B1) and aldosterone synthase (CYP11B2) gene expression in the rat central nervous system

2007 ◽  
Vol 196 (2) ◽  
pp. 305-311 ◽  
Author(s):  
Ping Ye ◽  
Christopher J Kenyon ◽  
Scott M MacKenzie ◽  
Katherine Nichol ◽  
Jonathan R Seckl ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adrenal Gland ◽  
Brain Regions ◽  
Dietary Sodium ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Aldosterone Synthase ◽  
The Central Nervous System ◽  
Wistar Kyoto

Using a highly sensitive quantitative RT-PCR method for the measurement of CYP11B1 (11β-hydroxylase) and CYP11B2 (aldosterone synthase) mRNAs, we previously demonstrated that CYP11B2 expression in the central nervous system (CNS) is subject to regulation by dietary sodium. We have now quantified the expression of these genes in the CNS of male Wistar Kyoto (WKY) rats in response to systemic ACTH infusion, dexamethasone infusion, and to adrenalectomy. CYP11B1 and CYP11B2 mRNA levels were measured in total RNA isolated from the adrenal gland and discrete brain regions using real-time quantitative RT-PCR. ACTH infusion (40 ng/day for 7 days, N=8) significantly increased CYP11B1 mRNA in the adrenal gland, hypothalamus, and cerebral cortex compared with animals infused with vehicle only. ACTH infusion decreased adrenal CYP11B2 expression but increased expression in all of the CNS regions except the cortex. Dexamethasone (10 μg/day for 7 days, N=8) reduced adrenal CYP11B1 mRNA compared with control animals but had no significant effect on either gene's expression in the CNS. Adrenalectomy (N=6 per group) significantly increased CYP11B1 expression in the hippocampus and hypothalamus and raised CYP11B2 expression in the cerebellum relative to sham-operated animals. This study confirms the transcription of CYP11B1 and CYP11B2 throughout the CNS and demonstrates that gene transcription is subject to differential regulation by ACTH and circulating corticosteroid levels.

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