Secretion of corticotrophin releasing factor from the adrenal during splanchnic nerve stimulation in conscious calves.

Edwards, A V; Jones, C. T.

doi:10.1113/jphysiol.1988.sp017112

Cited by 56 publications

(35 citation statements)

References 25 publications

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“…First, the range of CRH concentrations found to be effective on apoptosis was similar to the range believed to be present within the adrenal medulla (32)(33)(34)(35)(36). Second, normal chromaffin cells, like the PC12 cells, have specific CRH binding sites (37,38).…”

Section: Crh Induces Fas Ligand Production-serum Deprivation Induced mentioning

confidence: 94%

Corticotropin-releasing Hormone Induces Fas Ligand Production and Apoptosis in PC12 Cells via Activation of p38 Mitogen-activated Protein Kinase

Dermitzaki

Tsatsanis

Gravanis

et al. 2002

Journal of Biological Chemistry

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Recent experimental findings involve corticotropinreleasing hormone (CRH) in the cellular response to noxious stimuli and possibly apoptosis. The aim of the present work was to examine the effect of CRH on apoptosis and the Fas/Fas ligand system in an in vitro model, the PC12 rat pheochromocytoma cell line, which is widely used in the study of apoptosis and at the same time expresses the CRH/CRH receptor system. We have found the following. CRH induced Fas ligand production and apoptosis. These effects were mediated by the CRH type 1 receptor because its antagonist antalarmin blocked CRHinduced apoptosis and Fas ligand expression. CRH activated p38 mitogen-activated protein kinase, which was found to be essential for CRH-induced apoptosis and Fas ligand production. CRH also promoted a rapid and transient activation of ERK1/2, which, however, was not necessary for either CRH-induced apoptosis or Fas ligand production. Thus, CRH promotes PC12 apoptosis via the CRH type 1 receptor, which induces Fas ligand production via activation of p38.Several lines of evidence suggest that corticotropin-releasing hormone (CRH) 1 may play a role in the cellular response to noxious stimuli that promote neuron death (1). Indeed, CRH contributes to hippocampal ischemic injury, an effect prevented by the CRH antagonist ␣-helical CRH (ahCRH) (2). Similarly, astressin, a potent CRH antagonist, exerts a considerable neuroprotective effect on hippocampal cell damage following kainic acid-induced excitotoxic seizures (3). In animal models of induced status epilepticus, CRH causes neuronal loss in limbic structures, including the CA3 region of the hippocampus characterized by pyramidal cell apoptosis (4). Furthermore, administration of CRH to the brain of immature rats is associated with progressive hippocampal CA3 neuron apoptosis independent of glucocorticoids (5). These phenomena involve cell apoptosis. However, there is no information regarding the effects of CRH on the apoptotic machinery.The Fas/Fas ligand system controls apoptosis of several types of immune cells and possibly of epithelial and neural cells including cells in hippocampus and cortex (6, 7). The aim of the present work was to examine the effect of CRH on apoptosis and Fas ligand expression in a well established in vitro model, the PC12 rat pheochromocytoma cell line, which has characteristics of epithelial and neuronal cells and is widely used as a model in the study of apoptosis. PC12 cells express the CRH/ CRH receptor and the Fas/Fas ligand systems, providing a physiological model for the study of the effects of CRH on apoptosis and the intracellular signaling cascade involved (8, 9). When PC12 cells that are differentiated by nerve growth factor (NGF) are deprived of growth factors, they undergo apoptosis via expression of Fas ligand (10). Expression of Fas ligand and apoptosis in differentiated PC12 cells and primary cultures of rat sympathetic neurons depends on activation of stress-activated protein (SAP) kinase, p38 mitogen-activated protein kinase (MAPK), a...

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Section: Crh Induces Fas Ligand Production-serum Deprivation Induced mentioning

confidence: 94%

Corticotropin-releasing Hormone Induces Fas Ligand Production and Apoptosis in PC12 Cells via Activation of p38 Mitogen-activated Protein Kinase

Dermitzaki

Tsatsanis

Gravanis

et al. 2002

Journal of Biological Chemistry

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“…5,17 Within the adrenal itself, CRH-like immunoreactivity has been detected in the medulla of humans and other species. 18,19 This adrenal CRH is identical to the hypothalamic CRH and is released in response to physiological stimuli such as hemorrhage, 20 splanchnic nerve activation, 21,22 K + -induced depolarization, nicotine, 23 and various neuropeptides and cytokines. 24,25 Like the central CRH/ACTH system, the peripheral adrenal CRH/ACTH system is regulated via feedback mechMolecular Psychiatry anisms.…”

Section: Discussionmentioning

confidence: 99%

Effects of a novel corticotropin-releasing-hormone receptor type I antagonist on human adrenal function

et al. 2000

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“…3; Edwards & Jones, 1988). Adrenal cortical responses Stimulation of the peripheral end of the splanchnic nerve caused a steady rise in the concentration of ACTH in the arterial plasma which was associated with an increase in adrenal cortisol output and a rise in the concentration of cortisol in the peripheral plasma (Fig.…”

Section: Adrenal Medullary Responsesmentioning

confidence: 99%

“…ACTH and cortisol were measured by radioimmunoassay (Jones, Boddy, Robinson & Ratcliffe, 1977). Corticotrophin-releasing factor (CRF) was determined by radioimmunoassay as described previously (Edwards & Jones, 1988); the inter-and intra-assay coefficients of variation were 8 6 and 7-2 % respectively.…”

Section: Analytical Proceduresmentioning

confidence: 99%

Adrenal responses to splanchnic nerve stimulation in conscious calves given naloxone.

Edwards

Jones

1989

The Journal of Physiology

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SUMMARY1. The effects of stimulating the peripheral end of the right splanchnic nerve in the presence of naloxone (2 mg kg-') have been investigated in conscious 3 to 6-week-old calves.2. Mean aortic blood pressure rose to significantly higher levels during splanchnic stimulation in bursts at 40 Hz for 1 s at 10 s intervals than it did during stimulation at the corresponding continuous frequency (4 Hz). Furthermore, naloxone significantly reduced the fall in mean vascular resistance in response to both patterns of stimulation.3. The output of catecholamines from the adrenal gland, together with the proportion of noradrenaline released, was significantly enhanced by stimulating the splanchnic nerves in bursts in animals pre-treated with naloxone and the proportion of noradrenaline released also increased. In both cases the output of adrenaline and noradrenaline was within the same range as that reported previously in normal control animals.4. Naloxone significantly increased the amounts of enkephalin-like immunoreactivity and corticotrophin-releasing factor (CRF)-like immunoreactivity released from the adrenal gland in response to splanchnic nerve stimulation and raised the proportion of total to free met5-enkephalin that was secreted.5. Naloxone also inhibited the rise in plasma adrenocorticotrophic hormone (ACTH) concentration during continuous stimulation at 4 Hz, but not during stimulation at 40 Hz in bursts. Under these latter conditions the output of cortisol apparently directly from the adrenal gland was inhibited. The finding that splanchnic nerve stimulation can potentiate the output of cortisol in response to ACTH was confirmed.6. These results provide evidence that release of enkephalins and of CRF from the adrenal is inhibited by activating opioid receptors within the gland itself.

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Secretion of corticotrophin releasing factor from the adrenal during splanchnic nerve stimulation in conscious calves.

Cited by 56 publications

References 25 publications

Corticotropin-releasing Hormone Induces Fas Ligand Production and Apoptosis in PC12 Cells via Activation of p38 Mitogen-activated Protein Kinase

Corticotropin-releasing Hormone Induces Fas Ligand Production and Apoptosis in PC12 Cells via Activation of p38 Mitogen-activated Protein Kinase

Effects of a novel corticotropin-releasing-hormone receptor type I antagonist on human adrenal function

Adrenal responses to splanchnic nerve stimulation in conscious calves given naloxone.

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