Hemorrhage‐Induced Activations of Adrenocorticotropin Release and Catecholamine Metabolism in the Ventrolateral Medulla are Differently Affected by Glucocorticoid Feedback

@article{Ponec1992HemorrhageInducedAO,
  title={Hemorrhage‐Induced Activations of Adrenocorticotropin Release and Catecholamine Metabolism in the Ventrolateral Medulla are Differently Affected by Glucocorticoid Feedback},
  author={J. Ponec and Jo{\"e}l Lachuer and Marie-Françoise Suaud-Chagny and Marcel L. Tappaz},
  journal={Journal of Neuroendocrinology},
  year={1992},
  volume={4}
}
We have compared the effects of increasing doses of dexamethasone on the hemorrhage‐induced stimulation of the corticotropic axis and the metabolism of the catecholamines of the A1 group in the ventrolateral medulla. Adrenocorticotropin was measured in sequential samples of plasma while the metabolism of the catecholamines was recorded by in vivo electrochemistry in urethane‐anesthetized rats. Combined intracerebroventricular injection of specific adrenergic blockers (α1‐antagonist, prazosin… 
Differential time‐ and dose‐related effects of haemorrhage on tyrosine hydroxylase and neuropeptide Y mRNA expression in medullary catecholamine neurons
TLDR
The findings indicate that haemorrhage differentially affects TH and NPY expression in medullary catecholamine cell groups that participate in the maintenance of cardiovascular homeostasis and the prompt and robust NPY mRNA responses in adrenergic neurons suggests a mechanism by which peptide content of these cell groups' terminal projections is defended.
A comparison of two immediate-early genes, c-fos and NGFI-B, as markers for functional activation in stress-related neuroendocrine circuitry
TLDR
NGFI-B is established as a useful adjunct to c-fos, for revealing synaptic and/or transcriptional activation in the magno- and parvocellular neurosecretory systems.

References

SHOWING 1-10 OF 46 REFERENCES
Facilitation of immunoreactive corticotropin-releasing factor secretion into the hypophysial-portal circulation after activation of catecholaminergic pathways or central norepinephrine injection.
TLDR
Observations provide strong evidence in favor of a predominantly stimulatory action of NE (and possibly epinephrine) at the hypothalamic level to evoke secretion of CRF and thus to activate the pituitary-adrenal axis.
Lack of Glucocorticoids Enhances the Early Activation of the Medullary Catecholaminergic Cell Groups Triggered by Restraint Stress
We have investigated whether the stress‐induced activation of the medullary catecholaminergic neurons, that was shown previously to provide the main central activation input to the
Diurnal-stimulated and stress-induced ACTH release in rats is mediated by ventral noradrenergic bundle.
TLDR
Female rats were bilaterally injected with 3 micrograms of 6-hydroxydopamine dissolved in 0.2 microliter saline, via a glass micropipet stereotaxically implanted into the ventral noradrenergic-ascending bundle (VNAB), leading to pharmacological destruction of the VNAB and a striking decrease in the histofluorescence of hypothalamic catecholaminergic innervation.
Further evidence for a central stimulatory action of catecholamines on adrenocorticotropin release in the rat.
TLDR
A stress-like stimulatory dose response was noted after both adrenaline and noradrenaline infusions, with a half-maximal effect at concentrations of about 0.6 nmol and a maximal effect at 2.7 nmol or more, at maximally effective doses, adrenaline was significantly more active than norad Renaline.
Hemorrhage-induced secretion of corticotropin-releasing factor-like immunoreactivity into the rat hypophysial portal circulation and its inhibition by glucocorticoids.
TLDR
It is shown that CRF-LI is an important hypothalamic regulator of adenohypophysial ACTH secretion, and glucocorticoid negative feedback effects can be exerted at the central level.
Medullary lesions eliminate ACTH responses to hypotensive hemorrhage.
TLDR
It is demonstrated that lesions of the NTS eliminate the ACTH response to hemorrhage immediately and 4 days after the lesions but have no effect on resting ACTH levels.
Catecholaminergic modulation of corticotropin-releasing factor and adrenocorticotropin secretion.
TLDR
The responsiveness and physiological consequences of activation of these two systems are so inter-twined as to have generated the hypothesis that activation of the HPA is evoked by sympathoadrenomedullary activation.
Corticosteroid inhibition of ACTH secretion.
TLDR
There is some evidence that suggests that whereas comparator elements are not reset during stress, a comparator element is reset during the course of the circadian rhythm so that different basal levels of steroid are achieved.
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