Sex differences in body fluid homeostasis: Sex chromosome complement influences on bradycardic baroreflex response and sodium depletion induced neural activity

2015 ◽  
Vol 152 ◽  
pp. 416-421 ◽  
Author(s):  
L. Vivas ◽  
F.M. Dadam ◽  
X.E. Caeiro
Keyword(s):  
Sex Differences ◽  
Neural Activity ◽  
Body Fluid ◽  
Sex Chromosome ◽  
Chromosome Complement ◽  
Sodium Depletion ◽  
Fluid Homeostasis ◽  
Body Fluid Homeostasis

scholarly journals Effect of sex chromosome complement on sodium appetite and Fos-immunoreactivity induced by sodium depletion

2014 ◽  
Vol 306 (3) ◽  
pp. R175-R184 ◽  
Author(s):  
Florencia M. Dadam ◽  
Ximena E. Caeiro ◽  
Carla D. Cisternas ◽  
Ana F. Macchione ◽  
María J. Cambiasso ◽  
...  
Keyword(s):  
Sex Chromosome ◽  
Area Postrema ◽  
Brain Activity ◽  
Chromosome Complement ◽  
Circumventricular Organs ◽  
Sexually Dimorphic ◽  
Sodium Depletion ◽  
Sodium Diet ◽  
Sodium Appetite ◽  
Low Sodium Diet

Previous studies indicate a sex chromosome complement (SCC) effect on the angiotensin II-sexually dimorphic hypertensive and bradycardic baroreflex responses. We sought to evaluate whether SCC may differentially modulate sexually dimorphic-induced sodium appetite and specific brain activity due to physiological stimulation of the rennin angiotensin system. For this purpose, we used the “four core genotype” mouse model, in which the effect of gonadal sex and SCC is dissociated, allowing comparisons of sexually dimorphic traits between XX and XY females as well as in XX and XY males. Gonadectomized mice were sodium depleted by furosemide (50 mg/kg) and low-sodium diet treatment; control groups were administered with vehicle and maintained on normal sodium diet. Twenty-one hours later, the mice were divided into two groups: one group was submitted to the water-2% NaCl choice intake test, while the other group was perfused and their brains subjected to the Fos-immunoreactivity (FOS-ir) procedure. Sodium depletion, regardless of SCC (XX or XY), induced a significantly lower sodium and water intake in females than in males, confirming the existence in mice of sexual dimorphism in sodium appetite and the organizational involvement of gonadal steroids. Moreover, our results demonstrate a SCC effect on induced brain FOS-ir, showing increased brain activity in XX-SCC mice at the paraventricular nucleus, nucleus of the solitary tract, and lateral parabrachial nucleus, as well as an XX-SCC augmented effect on sodium depletion-induced brain activity at two circumventricular organs, the subfornical organ and area postrema, nuclei closely involved in fluid and blood pressure homeostasis.

Physiological regulation of the renal vasopressin receptor-effector pathway in dogs

1990 ◽  
Vol 258 (3) ◽  
pp. R763-R769
Author(s):  
L. B. Kinter ◽  
N. Caldwell ◽  
S. Caltabiano ◽  
C. Winslow ◽  
D. P. Brooks ◽  
...  
Keyword(s):  
Volume Expansion ◽  
Body Fluid ◽  
Physiological State ◽  
Extracellular Volume ◽  
Conscious Dogs ◽  
Physiological Regulation ◽  
Fluid Homeostasis ◽  
Effector Pathway ◽  
Body Fluid Homeostasis ◽  
V2 Receptor

Physiological regulation of receptor-effector pathways is recognized as a significant factor determining target organ selectivity and sensitivity in several hormonal systems. Whether or not physiological regulation of the renal vasopressin (V2) receptor-effector pathway participates in the control of body fluid homeostasis is unknown. We evaluated four states likely to be associated with altered sensitivities of the renal V2 receptor-effector pathway as follows: dehydration (18-h hydropenia), volume expansion, exogenous arginine vasopressin (AVP) infusion (10 ng/kg + 0.25 ng.kg-1.h-1), and cyclooxygenase blockade (indomethacin, 2 mg/kg + 2 mg.kg-1.h-1) for effects on the antidiuretic efficacies and potencies of putative V2-receptor antagonists in conscious dogs. The antidiuretic efficacies of desGly9[Pmp1-D-Tyr(Et)2Val4]AVP [Smith Kline & French (SK&F) 101926; 0.01-1,000 micrograms/kg] ranged from that of a full agonist to that of an antagonist, depending on the physiological state studied. The vasopressin antagonist potency of SK&F 101926 was increased 150-fold in association with extracellular volume expansion and decreased by blockade of renal cyclooxygenase activity. This spectrum of activities is that anticipated for a partial agonist under conditions where receptor number and/or sensitivity of receptor-effector coupling is increased or decreased, respectively. Thus volume expansion and increased circulating vasopressin concentration are associated with effective decreases, whereas hydropenia and cyclooxygenase blockade are associated with effective increases in sensitivity of the renal V2 receptor-effector pathway in the dog kidney. We conclude that the V2 receptor-effector pathway is a site of integration of physiological mechanisms participating in the control of body fluid homeostasis in conscious dogs.

scholarly journals Sex Differences in Ischemic Stroke Sensitivity Are Influenced by Gonadal Hormones, Not by Sex Chromosome Complement

2014 ◽  
Vol 35 (2) ◽  
pp. 221-229 ◽  
Author(s):  
Bharti Manwani ◽  
Kathryn Bentivegna ◽  
Sharon E Benashski ◽  
Venugopal Reddy Venna ◽  
Yan Xu ◽  
...  
Keyword(s):  
Sex Differences ◽  
Ischemic Stroke ◽  
Sex Hormones ◽  
Sex Chromosome ◽  
Chromosome Complement ◽  
Serum Testosterone ◽  
Gonadal Hormones ◽  
Epidemiologic Studies ◽  
Artery Occlusion ◽  
Male Mice

Epidemiologic studies have shown sex differences in ischemic stroke. The four core genotype (FCG) mouse model, in which the testes determining gene, Sry, has been moved from Y chromosome to an autosome, was used to dissociate the effects of sex hormones from sex chromosome in ischemic stroke outcome. Middle cerebral artery occlusion (MCAO) in gonad intact FCG mice revealed that gonadal males (XXM and XYM) had significantly higher infarct volumes as compared with gonadal females (XXF and XYF). Serum testosterone levels were equivalent in adult XXM and XYM, as was serum estrogen in XXF and XYF mice. To remove the effects of gonadal hormones, gonadectomized FCG mice were subjected to MCAO. Gonadectomy significantly increased infarct volumes in females, while no change was seen in gonadectomized males, indicating that estrogen loss increases ischemic sensitivity. Estradiol supplementation in gonadectomized FCG mice rescued this phenotype. Interestingly, FCG male mice were less sensitive to effects of hormones. This may be due to enhanced expression of the transgene Sry in brains of FCG male mice. Sex differences in ischemic stroke sensitivity appear to be shaped by organizational and activational effects of sex hormones, rather than sex chromosomal complement.

scholarly journals AT1a influences GABAA-mediated inhibition through regulation of KCC2 expression

2018 ◽  
Vol 315 (5) ◽  
pp. R972-R982 ◽  
Author(s):  
George E. Farmer ◽  
Kirthikaa Balapattabi ◽  
Martha E. Bachelor ◽  
Joel T. Little ◽  
J. Thomas Cunningham
Keyword(s):  
Protein Expression ◽  
Body Fluid ◽  
Neuronal Excitability ◽  
Receptor Activation ◽  
Cardiovascular Control ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Fluid Homeostasis ◽  
Body Fluid Homeostasis

The median preoptic nucleus (MnPO) is an integrative site involved in body fluid homeostasis, cardiovascular control, thermoregulation, and sleep homeostasis. Angiotensin II (ANG II), a neuropeptide shown to have excitatory effects on MnPO neurons, is of particular interest with regard to its role in body fluid homeostasis and cardiovascular control. The present study investigated the role of angiotensin type 1a (AT1a) receptor activation on neuronal excitability in the MnPO. Male Sprague-Dawley rats were infused with an adeno-associated virus with an shRNA against the AT1a receptor or a scrambled control. In vitro loose-patch voltage-clamp recordings of spontaneous action potential activity were made from labeled MnPO neurons in response to brief focal application of ANG II or the GABAA receptor agonist muscimol. Additionally, tissue punches from MnPO were taken to asses mRNA and protein expression. AT1a receptor knockdown neurons were insensitive to ANG II and showed a marked reduction in GABAA-mediated inhibition. The reduction in GABAA-mediated inhibition was not associated with reductions in mRNA or protein expression of GABAA β-subunits. Knockdown of the AT1a receptor was associated with a reduction in the potassium-chloride cotransporter KCC2 mRNA as well as a reduction in pS940 KCC2 protein. The impaired GABAA-mediated inhibition in AT1a knockdown neurons was recovered by bath application of phospholipase C and protein kinase C activators. The following study indicates that AT1a receptor activation mediates the excitability of MnPO neurons, in part, through the regulation of KCC2. The regulation of KCC2 influences the intracellular [Cl−] and the subsequent efficacy of GABAA-mediated currents.

Stanniocalcin-1 in the subfornical organ inhibits the dipsogenic response to angiotensin II

2012 ◽  
Vol 303 (9) ◽  
pp. R921-R928 ◽  
Author(s):  
Jason M. Moreau ◽  
Waseem Iqbal ◽  
Jeffrey K. Turner ◽  
Graham F. Wagner ◽  
John Ciriello
Keyword(s):  
Western Blot ◽  
Water Intake ◽  
Body Fluid ◽  
Physiological Role ◽  
Subfornical Organ ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Glycoprotein Hormone ◽  
Fluid Homeostasis ◽  
Body Fluid Homeostasis

Recently, receptors for the calcium-regulating glycoprotein hormone stanniocalcin-1 (STC-1) have been found within subfornical organ (SFO), a central structure involved in the regulation of electrolyte and body fluid homeostasis. However, whether SFO neurons produce STC-1 and how STC-1 may function in fluid homeostasis are not known. Two series of experiments were done in Sprague-Dawley rats to investigate whether STC-1 is expressed within SFO and whether it exerts an effect on water intake. In the first series, experiments were done to determine whether STC-1 was expressed within cells in SFO using immunohistochemistry, and whether protein and gene expression for STC-1 existed in SFO using Western blot and quantitative RT-PCR, respectively. Cells containing STC-1 immunoreactivity were found throughout the rostrocaudal extent of SFO. STC-1 protein expression within SFO was confirmed with Western blot, and SFO was also found to express STC-1 mRNA. In the second series, microinjections (200 nl) of STC-1, ANG II, a combination of the two or the vehicle were made into SFO in conscious, unrestrained rats. Water intake was measured at 0700 for a 1-h period after each injection in animals. Microinjections of STC-1 (17.6 or 176 nM) alone had no effect on water intake compared with controls. However, STC-1 not only attenuated the drinking responses to ANG II for about 30 min, but also decreased the total water intake over the 1-h period. These data suggest that STC-1 within the SFO may act in a paracrine/autocrine manner to modulate the neuronal responses to blood-borne ANG II. These findings also provide the first direct evidence of a physiological role for STC-1 in central regulation of body fluid homeostasis.

scholarly journals Breakdown of blood pressure and body fluid homeostasis in heart transplant recipients

1996 ◽  
Vol 27 (2) ◽  
pp. 375-383 ◽  
Author(s):  
Randy W. Braith ◽  
Roger M. Mills ◽  
Christopher S. Wilcox ◽  
Gary L. Davis ◽  
Charles E. Wood
Keyword(s):  
Blood Pressure ◽  
Heart Transplant ◽  
Body Fluid ◽  
Transplant Recipients ◽  
Fluid Homeostasis ◽  
Body Fluid Homeostasis ◽  
Heart Transplant Recipients

The role of thirst in body fluid homeostasis

Appetite ◽  
1989 ◽  
Vol 12 (1) ◽  
pp. 69-70
Author(s):  
David J. Ramsay ◽  
Terry Thrasher
Keyword(s):  
Body Fluid ◽  
Fluid Homeostasis ◽  
Body Fluid Homeostasis
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