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.

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.

scholarly journals The Effect of Herniarin on Spatial Working Memory, Pain Threshold, and Oxidative Stress in Ischemic Hypoperfusion Model in Rats

2021 ◽  
Vol 7 (1) ◽  
pp. 42-50
Author(s):  
Zahra Nazari Barchestani ◽  
◽  
Maryam Rafieirad ◽  
Keyword(s):  
Oxidative Stress ◽  
Pain Threshold ◽  
Male Rats ◽  
Control Group ◽  
Tail Flick ◽  
Pain Thresholds ◽  
Ischemic Group ◽  
Significant Difference ◽  
The Brain ◽  
And Oxidative Stress

Background: Ischemia causes severe neuronal damage and induces oxidative stress, memory impairment, and reduces pain threshold. Herniarin is a powerful antioxidant. Objectives: This study aimed to evaluate the effect of herniarin on memory, pain, and oxidative stress in an ischemia model in male rats. Materials & Methods: In this study, 50 male rats were divided into 5 groups of control, sham, ischemic, and two other ischemic groups, which received herniarin at doses of 150 and 300 mg/kg by gavage for 14 days. Behavioral tests were performed by shuttle box, and Y-maze and pain tests were performed by Tail-Flick test. Then, the rats’ brains were extracted to evaluate lipid peroxidation and measure the levels of thiol and Glutathione Peroxidase (GPX) in the hippocampus and striatum tissues. The results were expressed as Mean±SEM and then analyzed using suitable statistical methods of ANOVA and least significant difference post-hoc test in SPSS V. 20. Results: Herniarin significantly increased the avoidance memory, spatial memory, and pain thresholds of ischemic rats at different concentrations (P<0.001). Besides, the amount of malondialdehyde (MDA) and thiol in the ischemic group increased significantly in comparison to the control group (P<0.001). Also, in the ischemic group, GPX (P<0.001) significantly decreased. Decreased MDA (P<0.001) and thiol (P<0.001) and increased GPX levels were observed with herniarin administration (P<0.01). Conclusion: According to this study’s results, herniarin can remove free radicals and oxidant substances from the brain. Thus, it improves memory and pain thresholds in the brain hypoperfusion ischemia model.

scholarly journals Central interactions of aldosterone and angiotensin II in aldosterone- and angiotensin II-induced hypertension

2011 ◽  
Vol 300 (2) ◽  
pp. H555-H564 ◽  
Author(s):  
Baojian Xue ◽  
Terry G. Beltz ◽  
Yang Yu ◽  
Fang Guo ◽  
Celso E. Gomez-Sanchez ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Oxidase Inhibitor ◽  
Male Rats ◽  
Ang Ii ◽  
Adeno Associated Virus ◽  
Synergistic Interactions ◽  
Induced Hypertension ◽  
Ros Scavenger ◽  
The Brain

Many studies have implicated both angiotensin II (ANG II) and aldosterone (Aldo) in the pathogenesis of hypertension, the progression of renal injury, and cardiac remodeling after myocardial infarction. In several cases, ANG II and Aldo have been shown to have synergistic interactions in the periphery. In the present studies, we tested the hypothesis that ANG II and Aldo interact centrally in Aldo- and ANG II-induced hypertension in male rats. In rats with blood pressure (BP) and heart rate (HR) measured by DSI telemetry, intracerebroventricular (icv) infusions of the mineralocorticoid receptor (MR) antagonists spironolactone and RU28318 or the angiotensin type 1 receptor (AT1R) antagonist irbesartan significantly inhibited Aldo-induced hypertension. In ANG II-induced hypertension, icv infusion of RU28318 significantly reduced the increase in BP. Moreover, icv infusions of the reactive oxygen species (ROS) scavenger tempol or the NADPH oxidase inhibitor apocynin attenuated Aldo-induced hypertension. To confirm these effects of pharmacological antagonists, icv injections of either recombinant adeno-associated virus carrying siRNA silencers of AT1aR (AT1aR-siRNA) or MR (MR-siRNA) significantly attenuated the development of Aldo-induced hypertension. The immunohistochemical and Western blot analyses of AT1aR-siRNA- or MR-siRNA-injected rats showed a marked reduction in the expression of AT1R or MR in the paraventricular nucleus compared with scrambled siRNA rats. When animals from all studies underwent ganglionic blockade with hexamethonium, there was a smaller reduction in the fall of BP in animals receiving icv AT1R or MR antagonists. These results suggest that ANG II and Aldo interact in the brain in a mutually cooperative manner such that the functional integrity of both brain AT1R and MR are necessary for hypertension to be induced by either systemic ANG II or Aldo. The pressor effects produced by systemic ANG II or Aldo involve increased central ROS and sympathetic outflow.

scholarly journals Effects of dehydration on endocrine regulation of the electrolyte and fluid balance and atrial natriuretic peptide-binding sites in perinatally malnourished adult male rats

2002 ◽  
pp. 835-848 ◽  
Author(s):  
N Sebaai ◽  
J Lesage ◽  
A Alaoui ◽  
JP Dupouy ◽  
S Deloof
Keyword(s):  
Gene Expression ◽  
Binding Sites ◽  
Water Deprivation ◽  
Receptor Gene ◽  
Plasma Osmolality ◽  
Significant Rise ◽  
Male Rats ◽  
Receptor Density ◽  
D Values ◽  
Receptor Gene Expression

OBJECTIVE: The first aim of this work was to investigate, under basal conditions in adult male rats, the long-term consequences of perinatal maternal food restriction on the plasma concentrations of vasopressin (VP), aldosterone and atrial natriuretic peptide (ANP) and on plasma renin activity (PRA). Furthermore, under these same conditions, the hypothalamic VP gene expression as well as the density (B(max)), affinity (K(d)) and gene expression of ANP receptors were determined in kidneys and adrenals. The second aim of this work was to examine the responsiveness to dehydration in perinatally malnourished rats. Thus, the latter parameters were studied in these rats after 72 h water deprivation. METHODS: This study was conducted on 4-Month-old male rats from mothers exposed to 50% food restriction (FR50) during the last week of gestation and lactation and on age-matched control animals (C). At this stage, both C and FR50 rats were killed by decapitation between 0900 h and 1000 h in order to determine parameters under basal conditions or after 72 h water deprivation. Plasma VP, ANP and aldosterone levels and PRA were determined by radioimmunoassay. Hypothalamic VP gene expression was determined in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) by in situ hybridization. The B(max) and K(d) values of ANP receptors were evaluated from Scatchard plots. ANP receptor gene expression was determined by Northern blot analysis. RESULTS: Under basal conditions, perinatal malnutrition reduced body weight, absolute weight of kidneys and adrenals, and haematocrit. Compared with control rats, FR50 rats had significantly greater plasma VP and aldosterone levels but PRA, plasma ANP levels, plasma osmolality and hypothalamic VP gene expression were not significantly different. Perinatal malnutrition did not significantly affect glomerular ANP receptor density, but in adrenals it decreased both B(max) and K(d) values of ANP-B receptors (biological receptors) and increased B(max) of ANP-C receptors (clearance receptors). ANP-B(A) (receptor subtype A of ANP-B receptors) receptor gene expression was not significantly affected, whereas ANP-C receptor gene expression was enhanced in both adrenals and kidneys in FR50 rats. After 72 h dehydration, control rats showed a significant rise in haematocrit, plasma osmolality, PRA, circulating levels of VP and aldosterone and VP gene expression in both PVN and SON but showed a decrease in plasma ANP levels. B(max) of ANP-B receptors was decreased whereas B(max) of ANP-C receptors was enhanced in both adrenals and kidneys. ANP-B(A) receptor gene expression was not significantly affected in either kidneys or adrenals in dehydrated control rats. Similarly, ANP-C receptor gene expression was unaffected in kidneys whereas it was significantly enhanced in adrenals. In FR50 rats, the effects of water deprivation were qualitatively similar to those reported in controls concerning plasma parameters except for plasma VP levels which tended to rise (not significant) but this increase was only very slight compared with controls. Moreover, unlike controls, VP gene expression in both PVN and SON was not enhanced after dehydration in FR50 rats. In kidneys, dehydrated FR50 rats, like controls, upregulated ANP-C receptors, but they were unable to downregulate ANP-B receptors. In adrenals, unlike controls, FR50 rats enhanced ANP-B receptor density whereas they decreased both ANP-C receptor density and expression after 72 h dehydration. Similar to controls, the expression of ANP-B(A) receptors in both kidneys and adrenals as well as the expression of ANP-C receptors in kidneys, were unaffected in dehydrated FR50 rats. CONCLUSION: Perinatal malnutrition had long-lasting effects on regulation of the fluid and electrolyte balance under basal conditions. The main effects were a significant rise in circulating levels of VP and aldosterone, and changes in density of adrenal ANP-binding sites and ANP-C receptor gene expression in both adrenals and kidneys. Perinatal malnutrition also affects the responsiveness to water deprivation with alterations in both hypothalamic VP gene expression and regulation of ANP-binding sites.

scholarly journals CT Imaging and Spontaneous Behavior Analysis After Osmotic Blood-Brain Barrier Opening in Wistar Rat

2014 ◽  
pp. S529-S534 ◽  
Author(s):  
P. KOZLER ◽  
V. RILJAK ◽  
K. JANDOVÁ ◽  
J. POKORNÝ
Keyword(s):  
Locomotor Activity ◽  
Brain Edema ◽  
Brain Tissue ◽  
Blood Brain Barrier ◽  
Spontaneous Locomotor Activity ◽  
Brain Barrier ◽  
Male Rats ◽  
Blood Brain ◽  
Significant Difference ◽  
The Brain

In our previous experiments we demonstrated that osmotic opening of the blood brain barrier (BBB) in rats by administration of mannitol into the internal carotid artery leads to cerebral edema. The aim of this study was to confirm objectively the development of brain edema and determine whether it affects spontaneous locomotor activity in rats (SLA). Brain edema was verified by computer tomography (CT) examination of the brain and SLA was observed during open field test. Twenty four adult male rats were divided into four groups of six: (1) control animals (C), (2) controls with anesthesia (CA), (3) controls with sham surgery (CS), (4) experimental – osmotic opening of the BBB (MA). Osmotic BBB disruption manifested by reducing the density of brain tissue (hypodensity), suggesting a higher water content in the brain tissue. SLA was compared between C, CA, CS and MA groups and between MA and CA groups. Significant difference was found only between the control group and MA group. In the first 30 min of the examination, rats after the mannitol administration revealed a marked limitation of spontaneous locomotor activity. Experimental results demonstrated reduction of spontaneous locomotor activity in rats with induced brain edema.

Plasma vasopressin response to peripheral administration of angiotensin in conscious rats

1985 ◽  
Vol 248 (2) ◽  
pp. R249-R256 ◽  
Author(s):  
K. Yamaguchi ◽  
M. Koike ◽  
H. Hama
Keyword(s):  
Angiotensin Ii ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Plasma Sodium ◽  
Ang Ii ◽  
Mannitol Solution ◽  
Injection Volume ◽  
Conscious Rats ◽  
Plasma Vasopressin ◽  
Series Of Experiments

To assess a role for peripherally administered angiotensin II (ANG II) in regulating vasopressin (antidiuretic hormone, ADH) release, the effects on plasma ANG II and ADH of intraperitoneal injections of ANG II dissolved in various solutions were examined in conscious rats. Plasma ANG II and ADH were determined by radioimmunoassay using the trunk blood collected after decapitation. Injections of 150 mM NaCl containing ANG II (6, 12, or 24 micrograms X 2 ml-1 X 100 g body wt-1) caused dose-related increases in plasma ANG II 15 and 30 min after, but plasma ADH remained unchanged. The lack of effect on plasma ADH of the ANG II dissolved in isotonic saline was also confirmed in another series of experiments in which the solution with a higher ANG II concentration was loaded by much smaller injection volume (14.3 micrograms X 0.1 ml-1 X 100 g-1). However, when given together with 600 mM NaCl, ANG II (8 micrograms X 2 ml-1 X 100 g-1) significantly potentiated the plasma ADH response to the vehicle at 15, 30, and 60 min, without affecting those of plasma osmolality, sodium, and hematocrit. The elevations of plasma ANG II and osmolality brought about by the treatment were comparable with those previously observed in rats deprived of water for 46 h. ANG II was without effect on the plasma ADH responses to the intraperitoneal injections of hypertonic sucrose or mannitol solution that did not alter plasma sodium, although these solutions were equipotent to 600 mM NaCl in augmenting plasma ADH and osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

Estrogen receptor-α expression in osmosensitive elements of the lamina terminalis: regulation by hypertonicity

2004 ◽  
Vol 287 (3) ◽  
pp. R661-R669 ◽  
Author(s):  
Suwit J. Somponpun ◽  
Alan Kim Johnson ◽  
Terry Beltz ◽  
Celia D. Sladek
Keyword(s):  
Estrogen Receptor ◽  
Body Fluid ◽  
Water Deprivation ◽  
Plasma Osmolality ◽  
Significant Degree ◽  
Estrogen Receptor Α ◽  
Male Rats ◽  
Moderate Increase ◽  
Lamina Terminalis ◽  
Double Label

The subfornical organ (SFO), median preoptic nucleus (MnPO), and organum vasculosum lamina terminalis (OVLT), which are associated with the lamina terminalis, are important in the control of body fluid balance. Neurons in these regions express estrogen receptor (ER)-α, but whether the ER-α neurons are activated by hypertonicity and whether hypertonicity regulates ER-α expression are not known. Using fluorescent, double-label immunocytochemistry, we examined the expression of ER-α-immunoreactivity (ir) and Fos-ir in control and water-deprived male rats. In control animals, numerous ER-α-positive neurons were expressed in the periphery of the SFO, in both the dorsal and ventral MnPO, and in the dorsal cap of the OVLT. Fos-positive neurons were sparse in euhydrated rats but were numerous in the SFO, MnPO, and the dorsal cap of the OVLT after 48-h water deprivation. Most ER-α-ir neurons in these areas were positive for Fos, indicating a significant degree of colocalization. To examine the effect of dehydration on ER-α expression, animals with and without lesions surrounding the anterior and ventral portion of the 3rd ventricle (AV3V) were water deprived for 48 h. Water deprivation resulted in a moderate increase in ER-α-ir in the SFO of sham-lesioned rats ( P = 0.03) and a dramatic elevation in AV3V-lesioned animals ( P < 0.05). This was probably induced by the significant increase in plasma osmolality in both dehydrated groups ( P < 0.001) rather than a decrease in blood volume, because hematocrit was significantly increased only in the dehydrated sham-lesioned animals. Thus these studies implicate the osmosensitive regions of the lamina terminalis as possible targets for sex steroid effects on body fluid homeostasis.

Endocrine mechanisms regulating sodium excretion during water deprivation in dogs

1986 ◽  
Vol 251 (3) ◽  
pp. R560-R568 ◽  
Author(s):  
G. H. Metzler ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Sodium Excretion ◽  
Water Deprivation ◽  
Time Course ◽  
Plasma Osmolality ◽  
Plasma Aldosterone ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Potassium Excretion ◽  
Blood Samples ◽  
Plasma Vasopressin

The time course and mechanism of the natriuresis that accompanies 24 h of water, but not food, deprivation were studied in eight chronically catheterized dogs. Dogs were fed a controlled diet containing 35 meq of sodium, 110 meq of potassium, and 107 ml of water at 9:00 A.M. every day (time 0), and urine and blood samples were taken at 0, 2, 4, 6, 8, 10, 12, 16, 20, and 24 h after feeding on 3 consecutive days: the control, dehydration, and recovery days. Twenty-four hours of water deprivation decreased body weight by 880 g, increased plasma sodium by 7.2 meq, and increased plasma osmolality by 22.5 mosmol/kg. Cumulative daily sodium excretion increased from 30.4 +/- 2.8 meq on the control day to 50.7 +/- 5.7 meq on the dehydration day (P less than 0.01) and resulted in significant negative sodium balance that developed during the last half of the dehydration day. Cumulative sodium excretion during the first half of the dehydration day was not different from the corresponding period of the control day. Cumulative potassium excretion also increased from 91.9 +/- 4.5 meq during the control day to 123.0 +/- 6.7 meq during the dehydration day (P less than 0.01). Significant and progressive increases in plasma vasopressin concentration and renin activity were observed during water deprivation, but plasma aldosterone did not change from control levels. Furthermore, there was no correlation between the rate of sodium excretion and plasma vasopressin or aldosterone concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

cAMP in temperature- and ADH-regulating centers after thermal stress

1977 ◽  
Vol 42 (2) ◽  
pp. 257-261 ◽  
Author(s):  
I. Kornbluth ◽  
R. A. Siegel ◽  
N. Conforti ◽  
I. Chowers
Keyword(s):  
Thermal Stress ◽  
Heat Exposure ◽  
Plasma Osmolality ◽  
The Body ◽  
Neural Mechanisms ◽  
Male Rats ◽  
Paraventricular Nuclei ◽  
Regulate Body Temperature ◽  
Camp Levels ◽  
The Brain

cAMP concentrations in temperature-regulating sites of the brain and plasma osmolality were measured after exposure of male rats to 36 degrees C and 37–42% rh. for 10, 20, or 30 min. Plasma osmolality was affected by none of the heat exposures. In both the preoptic area and the posterior medial hypothalamus, cAMP concentrations were increased compared to controls, after 10, 20 and 30 min of heat exposure. In the supraoptic-paraventricular nuclei, neither 10 nor 20 min of exposure resulted in augmented cAMP concentrations; but after 30 min of heat exposure, cAMP levels in these nuclei were significantly greater than in controls. Neurohypophysial cAMP concentrations were increased after both 10 and 30 min of exposure. Cerebral cortical cAMP concentrations were not affected by thermal stress. It is concluded that cAMP is involved in the neural mechanisms which are brought into play to regulate body temperature during acute heat exposure. The significance of this involvement and its relation to the overall temperature-regulating mechanisms of the body are discussed.

A comparison of the dipsogenic responses of male and female rats to a variety of stimuli

1980 ◽  
Vol 58 (10) ◽  
pp. 1180-1183 ◽  
Author(s):  
Susan Kaufman
Keyword(s):  
Polyethylene Glycol ◽  
Angiotensin Ii ◽  
Water Deprivation ◽  
Sexual Difference ◽  
Female Rats ◽  
Male Rats ◽  
Male And Female ◽  
Fluid Compartment ◽  
Male And Female Rats ◽  
Extracellular Stimuli

Female rats subjected to 48 h of water deprivation drank more than similarly deprived males. There was no sexual difference in the dipsogenic responses to intracellular dehydration produced by intravenous hypertonic NaCl but females drank considerably more than males in response to the extracellular stimuli of hyperoncotic polyethylene glycol and angiotensin II. It is concluded that intact adult female rats are dipsogenically more responsive than adult male rats to stimuli acting through the pathways of extracellularly induced thirst but not to those arising from the intracellular fluid compartment.

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