scholarly journals Fetal Hypothalamus-Pituitary-Adrenal Responses to Estradiol Sulfate

Endocrinology ◽  
2011 ◽  
Vol 152 (12) ◽  
pp. 4966-4973 ◽  
Author(s):  
Charles E. Wood
Keyword(s):  
Fetal Brain ◽  
Control Group ◽  
Cortisol Secretion ◽  
Acth Secretion ◽  
Fetal Sheep ◽  
Adrenal Axis ◽  
Arterial Blood ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Near Term ◽  
Pituitary Adrenal Axis

Estradiol (E2) is an important modifier of the activity of the fetal hypothalamus-pituitary-adrenal axis. We have reported that estradiol-3-sulfate (E2SO4) circulates in fetal blood in far higher concentrations than E2 and that the fetal brain expresses steroid sulfatase, required for local deconjugation of E2SO4. We performed the present study to test the hypothesis that chronic infusion of E2SO4 chronically increases ACTH and cortisol secretion and that it shortens gestation. Chronically catheterized fetal sheep were treated with E2SO4 intracerebroventricular (n = 5), E2SO4 iv (n = 4), or no steroid infusion (control group, n = 5). Fetuses were subjected to arterial blood sampling every other day until spontaneous birth for plasma hormone analysis. Treatment with E2SO4 attenuated preparturient increases in ACTH secretion near term without affecting the ontogenetic rise in plasma cortisol. Infusion of E2SO4 intracerebroventricularly significantly increased plasma E2, plasma E2SO4, and plasma progesterone and shortened gestation compared with all other groups. These results are consistent with the conclusion that E2SO4: 1) interacts with the hypothalamus-pituitary-adrenal axis primarily by stimulating cortisol secretion and inhibiting ACTH and pro-ACTH secretion by negative feedback; and 2) stimulates the secretion of E2 and E2SO4. We conclude that the endocrine response to E2SO4 in the fetus is not identical with the response to E2.

Regulation of the hypothalamic–pituitary–adrenal axis in birth

1988 ◽  
Vol 66 (8) ◽  
pp. 1106-1112 ◽  
Author(s):  
A. N. Brooks ◽  
J. R. G. Challis
Keyword(s):  
Fetal Brain ◽  
Hypothalamic Pituitary Adrenal Axis ◽  
Adrenal Function ◽  
Pituitary Cells ◽  
Plasma Acth ◽  
Fetal Sheep ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal Axis ◽  
Pituitary Adrenal Axis

In sheep an increase in fetal pituitary–adrenal function, reflected in rising concentrations of plasma ACTH and cortisol, is important in relation to fetal organ maturation and the onset of parturition. This review presents evidence that implicates the hypothalamic–pituitary–adrenal axis in the control of parturition and describes recent experiments that explore in detail the maturation of the fetal hypothalamus and pituitary in relation to fetal adrenal function. Recent improvements for the measurement of ACTH in unextracted plasma and the ability to maintain vascular catheters in chronically catheterized fetal sheep have enabled subtle changes in fetal ACTH concentrations to be detected. As a result of these advances it has now been established that the terminal rise in cortisol, which is responsible for the onset of parturition in sheep, is preceded by an increase in fetal plasma ACTH concentrations. This has led to the hypothesis that birth results from the sequential development of the fetal hypothalamic–pituitary–adrenal axis with the signal originating from the fetal brain. This increase in trophic drive to the fetal adrenal may result from changes in the responsiveness of the fetal pituitary gland to factors that stimulate the release of ACTH. Corticotropin releasing factor (CRF) and arginine vasopressin are two such factors that stimulate the secretion of ACTH and cortisol secretion in the chronically catheterized fetal sheep. The response to these factors increases with gestational age and is sensitive to glucocorticoid feedback. Furthermore, repeated administration of CRF to immature fetal sheep results in pituitary and adrenal activation and in some cases may lead to premature parturition. Until recently, little was known of the controls of CRF secretion from the fetal hypothalamus. However, CRF has now been detected in the fetal sheep hypothalamus by radioimmunoassay and with immunohistochemistry, during the last third of pregnancy. The CRF material detected by radioimmunoassay co-elutes with synthetic ovine CRF on Sephadex G75 chromatography and also stimulates the release of ACTH from adult sheep pituitary cells maintained in culture. Furthermore at d100 of pregnancy (term of 145 days), CRF is released from fetal sheep hypothalami perifused in vitro both under basal conditions and in response to potassium-induced nerve terminal depolarization. Dexamethasone does not affect the release of CRF under these conditions. At d140, the hypothalamus contains similar quantities of immunoreactive and bioactive CRF which are released at a higher rate during in vitro perifusion. Potassium causes a similar release of CRF compared with d100 and again is unaffected by the presence of dexamethasone. However, at d140, dexamethasone does reduce basal CRF release. These results provide evidence for maturation of glucocorticoid feedback mechanisms at the level of the fetal hypothalamus and, together with the additional data presented in this review, illustrate the complexity of neuroendocrine control of the hypothalamic–pituitary–adrenal axis in birth.

Cerebrovascular autoregulation during fetal development in sheep

1994 ◽  
Vol 266 (3) ◽  
pp. H1069-H1074 ◽  
Author(s):  
S. Helou ◽  
R. C. Koehler ◽  
C. A. Gleason ◽  
M. D. Jones ◽  
R. J. Traystman
Keyword(s):  
Perfusion Pressure ◽  
Fetal Brain ◽  
Blood Gases ◽  
Fetal Sheep ◽  
Cerebrovascular Autoregulation ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Artificial Cerebrospinal Fluid ◽  
Near Term

There are scant data regarding the development of cerebrovascular autoregulation in fetuses. We tested the hypothesis that a decrease in cerebrovascular resistance (CVR) at reduced cerebral perfusion pressure (CPP) is absent in midgestation and near-term fetal sheep. Catheters were chronically implanted for microsphere determination of cerebral blood flow (CBF) in 9 fetuses at 92 days and in 10 fetuses at 132 days gestation (full term = 145 days). CPP was reduced by ventricular infusion of artificial cerebrospinal fluid. In 92-day fetuses, CPP was reduced stepwise from 35 to 25 and 18 mmHg and CBF decreased from 52 +/- 5 to 43 +/- 4 and 27 +/- 5 (SE) ml.min-1 x 100 g-1, respectively. Half of the immature fetuses showed some reduction in CVR at moderate reduction in CPP; however, there was no significant change in CVR in the group as a whole (from 0.72 +/- 0.06 to 0.61 +/- 0.04 and 0.89 +/- 0.20 mmHg.ml-1.min.100 g). In 132-day fetuses, CPP was reduced from 45 to 33 and 28 mmHg and CBF was unchanged (from 105 +/- 7 to 97 +/- 11 and 89 +/- 8 ml.min-1 x 100 g-1). CVR decreased from 0.45 +/- 0.05 to 0.41 +/- 0.08 and 0.33 +/- 0.03 mmHg.ml-1.min.100 g. There were no significant changes in arterial blood gases at reduced CPP in either age group. We conclude that cerebrovascular autoregulation at reduced CPP is not well developed at 92 days (0.63 gestation) in fetal sheep but that autoregulatory capacity is evident near term. We speculate that poor autoregulation may place the premature fetal brain at risk for injury.

scholarly journals Acupuncture blocks cold stress-induced increases in the hypothalamus–pituitary–adrenal axis in the rat

2013 ◽  
Vol 217 (1) ◽  
pp. 95-104 ◽  
Author(s):  
Ladan Eshkevari ◽  
Eva Permaul ◽  
Susan E Mulroney
Keyword(s):  
Cold Stress ◽  
Chronic Stress ◽  
Stress Hormones ◽  
Control Group ◽  
Adrenal Axis ◽  
Significant Difference ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
The Brain ◽  
Treatment Control Group ◽  
Pituitary Adrenal Axis

Electroacupuncture (EA) is used to treat chronic stress; however, its mechanism(s) of action in allaying stress remains unclear. The interplay of stress hormones of the hypothalamus–pituitary–adrenal axis (HPA) and the sympathetic nervous system (SNS) is critical in the stress response. Our objective was to determine whether EA at acupoint, stomach 36 (EA St36) is effective in preventing chronic cold stress-induced increased hormone levels in the rat by examining four groups of animals, three of which were exposed to cold and one of which was a non-treatment control group. Before exposure to the cold, two groups were treated with either EA St36, or Sham-EA, before 10 days of cold stress. The EA St36 animals demonstrated a significant decrease in peripheral HP hormones (ACTH and CORT) compared with stress animals (P<0.05). These effects were specific; rats receiving Sham-EA had elevation of these hormones, similar to the stress-only animals. These effects were mirrored centrally in the brain; CRH levels were significantly (P<0.05) reduced in EA St36 animals compared with the other animals. Finally, EA effect on peripheral and adrenal SNS hormones (norepinephrine (NE) and neuropeptide Y (NPY) respectively) was examined, with no significant difference noted in adrenal tyrosine hydroxylase or circulating NE in any of the groups. However, EA St36 was effective in preventing stress-induced elevation is adrenal Npy mRNA. These results indicate that EA St36 blocks the chronic stress-induced elevations in the HPA and the sympathetic NPY pathway, which may be a mechanism for its specific stress-allaying effects.

Low-dose flunarizine does not affect short-term fetal circulatory responses to acute asphyxia in sheep near term

1998 ◽  
Vol 10 (5) ◽  
pp. 405 ◽  
Author(s):  
Yves Garnier ◽  
Richard Berger ◽  
Doris Pfeiffer ◽  
Arne Jensen
Keyword(s):  
Low Dose ◽  
Plasma Concentrations ◽  
Neuronal Cell ◽  
Cardiovascular Responses ◽  
Control Group ◽  
Short Term ◽  
Fetal Sheep ◽  
Physiological Variables ◽  
Arterial Blood ◽  
Near Term

Asphyxia is one of the major causes of perinatal brain damage and neuronal cell loss, which may result in psychomotor deficits during later development. It has been shown previously that the immature brain can be protected from ischemic injury by flunarizine, a class IV calcium antagonist. However, cardiovascular side-effects of flunarizine, when applied at the dosages used in those studies, have been reported. Recently, the present authors were able to demonstrate that even by injecting flunarizine at a far lower dosage (1 mg kg) estimated bodyweight) neuronal cell damage, caused by occlusion of both carotid arteries for 30 min, can be reduced in fetal sheep near term. The aim of the present study was, therefore, to examine whether low-dose flunarizine affects fetal cardiovascular responses to acute asphyxia in sheep near term. Ten fetal sheep were chronically instrumented at a mean gestational age of 132 1 days (term is at 147 days). Fetuses from the study group received a bolus injection of flunarizine (1 mg kg–1 estimated fetal weight) 60 min before asphyxia, whereas the solvent was administered to the fetuses from the control group. Organ blood flows, physiological variables and plasma concentrations of catecholamines were measured before, during and after a single occlusion of uterine blood flow for 2 min (i.e. at 0, 1, 2, 3, 4, and 30 min). Before asphyxia, the distribution of combined ventricular output and physiological variables, as well as concentrations of catecholamines, in fetuses from the control group were in the normal range for chronically prepared fetal sheep near term. During acute asphyxia there was a redistribution of cardiac output towards the central organs accompanied by a pronounced bradycardia and a rapid increase in arterial blood pressure. After asphyxia circulatory centralization did not resolve quite as rapidly as it developed, but was almost completely recovered at 30 min after the insult. There were nearly no differences in the time course of physiological and cardiovascular variables measured before, during and after acute intrauterine asphyxia between the control and study groups. From the present study it was concluded that low-dose flunarizine does not affect short-term fetal circulatory responses to acute asphyxia in sheep near term.

scholarly journals QT Interval Instability and Variability in Dogs with Hyperadrenocorticism

2021 ◽  
Author(s):  
Beatriz de Carvalho Pato Vila ◽  
Marcela Sigolo Vanhoni ◽  
Marlos Gonçalves Sousa
Keyword(s):  
Qt Interval ◽  
Statistical Difference ◽  
Ventricular Repolarization ◽  
Control Group ◽  
Short Term ◽  
Adrenal Axis ◽  
Electrical Instability ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Electrocardiographic Parameters ◽  
Pituitary Adrenal Axis

Abstract Hyperadrenocorticism is one of the most common endocrine diseases in dogs. In humans, it is clearly associated with a higher risk of cardiovascular events, but studies in dogs are scarce. To investigate the arrhythmogenic risk of dogs with hyperadrenocorticism, indices of variability and instability of the QT interval were studied in 38 dogs with hyperadrenocorticism and in 12 healthy dogs: variance (QTv), total instability (TI), short-term (STI) and long-term (LTI), and mean (QTm). Except for QTm, all parameters studied were higher in the hyperadrenocorticism group than in the control group. In addition, STI and QTv showed moderate positive correlation with left ventricle wall thickness. To a better understanding on the effect of the hypothalamus-pituitary-adrenal axis on ventricular repolarization, the hyperadrenocorticism group was subdivided according to the percentage of variation in plasma cortisol concentration (<30.1%; 30.1-60%; >60%) 8 hours after low-dose administration of dexamethasone. There was statistical difference in QTv, TI and LTI indices between the control group and the <30.1% and >60% groups, and in STI index between the control group and the >60% group. There was no statistical difference between sex groups in any of the electrocardiographic parameters studied. This result may indicate that the etiology of hyperadrenocorticism, and its consequent influence on hypothalamus-pituitary-adrenal axis could interfere on the heterogeneity of ventricular repolarization parameters in different ways, especially in the short-term stability; however further studies are necessary to understand the role of cortisol on electrical instability in dogs.

Deciphering the Association Between Hypothalamus‐Pituitary‐Adrenal Axis Activity and Obesity: A Meta‐Analysis

Obesity ◽  
2021 ◽  
Author(s):  
Giada Ostinelli ◽  
Anaïs Scovronec ◽  
Sylvain Iceta ◽  
Anne‐Sophie Ouellette ◽  
Simone Lemieux ◽  
...  
Keyword(s):  
Meta Analysis ◽  
Adrenal Axis ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis

Contribution of Growth Arrest-Specific 5/miR-674 to the Hypothalamus Pituitary Adrenal Axis Regulation Effect by Electroacupuncture following Trauma

2021 ◽  
pp. 1-13
Author(s):  
Jing Zhu ◽  
Chunxia Guo ◽  
Pingping Lu ◽  
Shuijin Shao ◽  
Bing Tu
Keyword(s):  
Hpa Axis ◽  
Interleukin 1 ◽  
Growth Arrest ◽  
Luciferase Assay ◽  
Function Evaluation ◽  
Protein Levels ◽  
Adrenal Axis ◽  
Post Surgery ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis

<b><i>Background:</i></b> Electroacupuncture (EA) can improve trauma-induced hypothalamus pituitary adrenal axis (HPA) hyperactivity. However, the mechanism underlying the EA effect has not been fully understood. <b><i>Methods and Study Design:</i></b> This study was undertaken to explore the role of hypothalamic growth arrest-specific 5 (Gas5) in the regulation of EA on HPA axis function post-surgery. Paraventricular nuclear Gas5 levels were upregulated in rats using an intracerebroventricular injection of pAAV-Gas5. Primary hypothalamic neurons and 293T cells were cultured for miRNA and siRNAs detection. Radioimmunoassay, PCR, Western blot, and immunohistochemistry were used for HPA axis function evaluation. <b><i>Results:</i></b> The overexpression of Gas5 abolished the effect of EA on the regulation of trauma-induced HPA axis hyperactivity. Using a bioinformatics analysis and dual luciferase assay, we determined that miRNA-674 was a target of Gas5. Additionally, miRNA-674 levels were found to have decreased in trauma rats, and this effect was reversed after EA intervention. TargetScan analysis showed that serum and glucocorticoid inducible kinase 1 (SGK1) were targets of miR-674. Moreover, we found that SGK1 protein levels increased in trauma rats and SGK1 expression inhibition alleviated HPA axis abnormality post-surgery. EA could improve the number of hypothalamus iba-1 positive cells and hypothalamic interleukin 1 beta protein expression. <b><i>Conclusions:</i></b> Our study demonstrated the involvement of the hypothalamic Gas5/miRNA-674/SGK1 signaling pathway in EA regulation of HPA axis function after trauma.

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