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.

scholarly journals Effects of Acupuncture, RU-486 on the Hypothalamic-Pituitary-Adrenal Axis in Chronically Stressed Adult Male Rats

Endocrinology ◽  
2015 ◽  
Vol 156 (10) ◽  
pp. 3649-3660 ◽  
Author(s):  
Ladan Eshkevari ◽  
Susan E. Mulroney ◽  
Rupert Egan ◽  
Lixing Lao
Keyword(s):  
Cold Stress ◽  
Adult Male ◽  
Stress Responses ◽  
Male Rats ◽  
Control Group ◽  
Ru 486 ◽  
Adrenal Axis ◽  
Stomach Meridian ◽  
Anxious Behavior ◽  
Pituitary Adrenal Axis

We have recently reported that pretreatment with electroacupuncture (EA) at stomach meridian point 36 (St36) prevents the chronic cold-stress increase in the hypothalamus-pituitary-adrenal axis (HPA), an action that may be under central control. Given that treatment for stress-related symptoms usually begins after onset of the stress responses, the objectives of the present study were to determine the efficacy of EA St36 on HPA hormones when EA St36 is given after stress was initiated, if the results are long lasting, and if blocking the glucocorticoid receptor (GR) using RU-486 had the same effects as EA St36. Adult male rats were placed in 4 groups of animals, 3 of which were exposed to cold and 1 of which was a nontreatment control group. After exposure to the cold stress, 2 groups were treated with either EA St36 or sham-EA, repeated over 10 days. The increase in ACTH and corticosterone observed in stress-only rats was prevented in EA St36 animals, and the effects remained intact 4 days after withdrawal of EA but continuation of cold stress. When the GR was blocked with RU-486, the efficacy of EA St36 remained unchanged. GR blockade did significantly elevate ACTH, which is not seen with EA St36, suggesting that EA St36 does act centrally. The elevated HPA hormones in stress-only rats were associated with a significant increase in depressive and anxious behavior; this was not observed in the stressed EA St36 animals. The results indicate that EA specifically at St36 vs sham-EA is effective in treating chronic poststress exposure.

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.

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.

scholarly journals The Hypothalamic-Pituitary-Adrenal Axis Response to Stress in Mice Lacking Functional Vasopressin V1b Receptors

Endocrinology ◽  
2007 ◽  
Vol 148 (2) ◽  
pp. 849-856 ◽  
Author(s):  
Stephen J. Lolait ◽  
Lesley Q. Stewart ◽  
David S. Jessop ◽  
W. Scott Young ◽  
Anne-Marie O’Carroll
Keyword(s):  
Chronic Stress ◽  
Hypothalamic Pituitary Adrenal Axis ◽  
Wild Type ◽  
Plasma Acth ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal Axis ◽  
Significant Difference ◽  
Response To Stress ◽  
Pituitary Adrenal Axis

The role of arginine vasopressin (Avp) as an ACTH secretagogue is mediated by the Avp 1b receptor (Avpr1b) found on anterior pituitary corticotropes. Avp also potentiates the actions of CRH (Crh) and appears to be an important mediator of the hypothalamic-pituitary-adrenal axis response to chronic stress. To investigate the role of Avp in the hypothalamic-pituitary-adrenal axis response to stress, we measured plasma ACTH and corticosterone (CORT) levels in Avpr1b knockout (KO) mice and wild-type controls in response to two acute (restraint and insulin administration) and one form of chronic (daily restraint for 14 d) stress. No significant difference was found in the basal plasma levels of ACTH and CORT between the two genotypes. Acute restraint (30 min) increased plasma ACTH and CORT to a similar level in both the Avpr1b mutant and wild-type mice. In contrast, plasma ACTH and CORT levels induced by hypoglycemia were significantly decreased in the Avpr1b KO mice when compared with wild-type littermates. There was no difference in the ACTH response to acute and chronic restraint in wild-type mice. In the Avpr1b KO group subjected to 14 sessions of daily restraint, plasma ACTH was decreased when compared with wild-type mice. On the other hand, the CORT elevations induced by restraint did not adapt in the Avpr1b KO or wild-type mice. The data suggest that the Avpr1b is required for the normal pituitary and adrenal response to some acute stressful stimuli and is necessary only for a normal ACTH response during chronic stress.

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