Effects of Water-Deprivation on Aldosterone Production in Brattleboro Male Rats Congenitally Lacking Vasopressin

1985 ◽  
Vol 17 (05) ◽  
pp. 230-233 ◽  
Author(s):  
E. Ezzarani ◽  
J. Laulin ◽  
R. Brudieux
2020 ◽  
Vol 318 (3) ◽  
pp. R567-R578 ◽  
Author(s):  
Susana Quirós Cognuck ◽  
Wagner L. Reis ◽  
Marcia S. Silva ◽  
Gislaine Almeida-Pereira ◽  
Lucas K. Debarba ◽  
...  

Maintenance of the volume and osmolality of body fluids is important, and the adaptive responses recruited to protect against osmotic stress are crucial for survival. The objective of this work was to compare the responses that occur in aging male and female rats during water deprivation. For this purpose, groups of male and female Wistar rats aged 3 mo (adults) or 18 mo (old) were submitted to water deprivation (WD) for 48 h. The water and sodium (0.15 M NaCl) intake, plasma concentrations of oxytocin (OT), arginine vasopressin (AVP), corticosterone (CORT), atrial natriuretic peptide (ANP), and angiotensin II (ANG II) were determined in hydrated and water-deprived animals. In response to WD, old male and female rats drank less water and saline than adults, and both adult and old females drank more water and saline than respective males. Dehydrated old animals displayed lower ANG II plasma concentration and CORT response compared with the respective normohydrated rats. Dehydrated adult males had higher plasma ANP and AVP as well as lower CORT concentrations than dehydrated adult females. Moreover, plasma OT and CORT levels of old female rats were higher than those in the dehydrated old male rats. Relative expression of ANG II type 1 receptor mRNA was decreased in the subfornical organ of adult and old male rats as well as adult female rats in response to WD. In conclusion, the study elucidated the effect of sex and age on responses induced by WD, altering the degree of dehydration induced by 48 h of WD.


2002 ◽  
pp. 835-848 ◽  
Author(s):  
N Sebaai ◽  
J Lesage ◽  
A Alaoui ◽  
JP Dupouy ◽  
S Deloof

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.


1980 ◽  
Vol 93 (4) ◽  
pp. 407-412 ◽  
Author(s):  
K. Yamaguchi ◽  
H. Hama ◽  
T. Sakaguchi ◽  
H. Negoro ◽  
K. Kamoi

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.


2004 ◽  
Vol 287 (3) ◽  
pp. R661-R669 ◽  
Author(s):  
Suwit J. Somponpun ◽  
Alan Kim Johnson ◽  
Terry Beltz ◽  
Celia D. Sladek

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.


1982 ◽  
Vol 99 (4) ◽  
pp. 493-499 ◽  
Author(s):  
G. Valiquette ◽  
L. Martini

Abstract. The secretion of vasopressin has been shown recently to be influenced by gonadal steroids. To further evaluate the relevance of sex steroids in the control of vasopressin secretion, the vasopressin response to dehydration has been studied in normal, castrated and sex-steroid treated castrated male rats. Short-term (3 weeks) castration did not modify the vasopressin response to 48 h of water deprivation. Long-term (10 weeks) castration, on the other hand, consistently reduced the vasopressin response by more than 50%. In both cases, the osmolality was unaffected. Treatment of long-term castrated rats with testosterone, dihydrotestosterone, or oestradiol increased the vasopressin response to dehydration towards normal control levels. However, only oestradiol could restore it to and beyond normal levels, although all three steroids were given in doses that were equipotent in bringing back to normal the plasma LH levels of the castrated animals. Angiotensin-II generation may indirectly be augmented by oestradiol treatment and this may account for the effect of oestradiol here reported. No such mechanism, however, may be invoked in the case of androgens; a direct modulatory effect at the hypothalamic level is postulated for explaining their influence on vasopressin secretion.


1980 ◽  
Vol 58 (10) ◽  
pp. 1180-1183 ◽  
Author(s):  
Susan Kaufman

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.


2005 ◽  
Vol 288 (1) ◽  
pp. R311-R321 ◽  
Author(s):  
Lisa L. Ji ◽  
Tiffany Fleming ◽  
Maurice L. Penny ◽  
Glenn M. Toney ◽  
J. Thomas Cunningham

We studied cFos and FosB staining in the supraoptic nucleus (SON) the organum vasculosum of the lamina terminalis (OVLT) and the median preoptic nucleus (MnPO) in adult male rats after water deprivation (24 h, n = 11; 48 h, n = 12) and water deprivation with rehydration (22 h + water, n = 11; 46 h + water, n = 10). Control rats ( n = 15) had water available ad libitum. Separate sets of serial sections from each brain were processed for immunocytochemistry using primary antibodies against either c-Fos or FosB protein. Plasma osmolality, vasopressin, hematocrit, and plasma proteins were measured in separate groups ( n = 6–7). The number of c-Fos-positive cells in the SON was significantly increased after 24 and 48 h of water deprivation. In contrast, rehydrated groups were not different from control. Water deprivation significantly increased c-Fos staining in both the OVLT and the MnPO, but c-Fos staining was not altered by rehydration. FosB staining in the SON was significantly increased only by 48-h water deprivation, and this effect was significantly decreased by rehydration. In the MnPO and OVLT, FosB staining was significantly increased by water deprivation, and, like c-Fos staining, these increases were not affected by rehydration. Water deprivation significantly increased osmolality and hematocrit, as well as plasma protein and vasopressin concentrations. Plasma measurements from rehydrated rats were not different from control. We conclude that water deprivation and rehydration differentially affect c-Fos and FosB staining in a region-dependent manner.


Metabolism ◽  
1999 ◽  
Vol 48 (9) ◽  
pp. 1108-1114 ◽  
Author(s):  
Mei-Mei Kau ◽  
Ming-Jae Lo ◽  
Shyi-Wu Wang ◽  
Shiow-Chwen Tsai ◽  
Jiann-Jong Chen ◽  
...  

1959 ◽  
Vol 197 (1) ◽  
pp. 173-176 ◽  
Author(s):  
Carl S. Alexander

Water and salt loading experiments were carried out on normal male rats and rats with chronic diabetes insipidus (DI). The effect of two additional variables has been studied, i.e. that of withholding food and water prior to loading and that of the route of administration of the load (oral or intraperitoneal). Water deprivation prior to water loading reduced the excretion of water by DI animals far below that of normal rats regardless of the route of administration. Salt loading, on the contrary, obviated the influence of prior water deprivation and in every instance DI animals excreted more of the load as compared to controls. The quantitative but not qualitative excretion of both a water and saline load was affected when the intraperitoneal route was used. In both normal and DI rats potassium excretion far exceeded the output of sodium and chloride during water loading regardless of prior food and water deprivation. Desoxycorticosterone acetate (DCA) enhanced sodium excretion in saline loaded hydropenic normal rats but failed to influence sodium excretion in DI rats. Pitressin failed to produce an antidiuretic effect during saline diuresis; however, there was a marked increase in the excretion of salt and potassium in both DI and normal animals.


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