The Corticotropin-Releasing Factor Release in Rat Hypophysial Portal Blood Is Mediated by Brain Catecholamines

Guillaume, Viviane; Conte-Devolx, B.; Szafarczyk, A.; Malaval, F.; Parés‐Herbuté, Núria; Grino, Michel; Alonso, Gérard; Assenmacher, I; Oliver, Charles

doi:10.1159/000124811

Cited by 118 publications

(53 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These observations suggest that the IIH-induced CRF and AVP release into HPB is mediated through extrahypothalamic pathways. We and others have shown recently that central catecholamines, originating from the brainstem nuclei, have a stimulatory effect on hypothalamic CRF secretion in the rat (27,28). Interestingly, hypothalamic norepinephrine activity is increased during IIH in rats, and this increase parallels the variation in plasma corticosterone (29).…”

Section: Ram N 566mentioning

confidence: 70%

Insulin-induced hypoglycemia stimulates corticotropin-releasing factor and arginine vasopressin secretion into hypophysial portal blood of conscious, unrestrained rams.

Caraty¹,

Grino²,

Locatelli³

et al. 1990

J. Clin. Invest.

132

View full text Add to dashboard Cite

Insulin-induced hypoglycemia (IIH) is a strong stimulator of pituitary ACI`H secretion. The mechanisms by which IIH activates the corticotrophs are still controversial. Indeed, in rats the variations of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) secretion in hypophysial portal blood (HPB) during IIH have been diversely appreciated. This may be due to the stressful conditions required for portal blood collection in rats. We studied the effects of IIH on the secretion of CRF and AVP in HPB and on the release of ACTH and cortisol in peripheral plasma in conscious, unrestrained, castrated rams. After the injection of a low (0.2 IU/kg) or high dose (2 IU/kg) of insulin, AC'TH and cortisol levels in peripheral plasma increased in a dose-related manner. After injection of the low dose of insulin, CRF and AVP secretion in HPB were equally stimulated. After injection of the high dose of insulin, CRF secretion was further stimulated, while AVP release was dramatically increased. These results suggest that when the hypoglycemia is moderate, CRF is the main factor triggering ACITI release, and that the increased AVP secretion potentiates the stimulatory effect of CRF. When hypoglycemia is deeper, AVP secretion becomes predominant and may by itself stimulate ACTH release. (J. Clin. Invest. 1990.

show abstract

Section: Ram N 566mentioning

confidence: 70%

Insulin-induced hypoglycemia stimulates corticotropin-releasing factor and arginine vasopressin secretion into hypophysial portal blood of conscious, unrestrained rams.

Caraty¹,

Grino²,

Locatelli³

et al. 1990

J. Clin. Invest.

132

View full text Add to dashboard Cite

show abstract

“…Furthermore, catecholamines are known to influence the activity of neurons in the brain including the PGi and the CNA (Clayton and Williams, 2000;Williams et al, 2000). The PGi and CNA are enriched with corticotropin releasing factor (CRF) synthesizing neurons (Swanson et al, 1983;Herbert and Saper, 1990;Grigson et al, 1997a;Van Bockstaele et al, 1998b;Van Bockstaele et al, 1999) and it has been shown that norepinephrine influences the release of CRF (Guillaume et al, 1987;Koob, 1999) and adrenocorticotrophic hormone (Szafarczyk et al, 1987). Taken together, NTS neurons may coordinate the autonomic regulation of the limbic and amygdalar brain regions via targeting CRF neurons in these regions.…”

Section: Discussionmentioning

confidence: 99%

Divergent projections of catecholaminergic neurons in the nucleus of the solitary tract to limbic forebrain and medullary autonomic brain regions

Reyes

Bockstaele

2006

Brain Research

View full text Add to dashboard Cite

The nucleus of the solitary tract (NTS) is a critical structure involved in coordinating autonomic and visceral activities. Previous independent studies have demonstrated efferent projections from the NTS to the nucleus paragigantocellularis (PGi) and the central nucleus of the amygdala (CNA) in rat brain. To further characterize the neural circuitry originating from the NTS with postsynaptic targets in the amygdala and medullary autonomic targets, distinct green or red fluorescent latex microspheres were injected into the PGi and the CNA, respectively, of the same rat. Thirty-micron thick tissue sections through the lower brainstem and forebrain were collected. Every fourth section through the NTS region was processed for immunocytochemical detection of tyrosine hydroxylase (TH), a marker of catecholaminergic neurons. Retrogradely labeled neurons from the PGi or CNA were distributed throughout the rostro-caudal segments of the NTS. However, the majority of neurons containing both retrograde tracers were distributed within the caudal third of the NTS. Cell counts revealed that approximately 27% of neurons projecting to the CNA in the NTS sent collateralized projections to the PGi while approximately 16% of neurons projecting to the PGi sent collateralized projections to the CNA. Interestingly, more than half of the PGi and CNA projecting neurons in the NTS expressed TH immunoreactivity. These data indicate that catecholaminergic neurons in the NTS are poised to simultaneously coordinate activities in limbic and medullary autonomic brain regions.

show abstract

“…Amongst the monoamines controlling CRF and AVP are noradrenaline and 5-hydroxytryptamine. Lesioning of these monoaminergic pathways [4][5][6] or modification of 5-HT activity [7] alters the release of CRF in animal models.…”

Section: Introductionmentioning

confidence: 99%

The effects of oral sumatriptan, a 5‐HT1 receptor agonist, on circulating ACTH and cortisol concentrations in man.

Entwisle

Fowler

Thomas

et al. 1995

Brit J Clinical Pharma

View full text Add to dashboard Cite

1 The effects of oral sumatriptan (50, 100 and 200 mg), a 5-HT1 receptor agonist, and placebo, on circulating adrenocorticotrophic hormone (ACTH) and cortisol concentrations were determined over 24 h after dosing, in 26 healthy male subjects. ACTH was measured by immunoradiometric assay and cortisol by radioimmunoassay. 2 After sumatriptan all subjects displayed a normal diurnal rhythm for circulating ACTH and cortisol compared with placebo. 3 There was a reduction in the trough circulating ACTH concentration over 0-4 h which was 18% with 100 mg (P = 0.002), and 25% with 200 mg (P < 0.001).The 5 h, post-prandial, peak ACTH concentration was reduced by 21% with 100 mg (P = 0.018) and by 20% with 200 mg (P = 0.024). The weighted mean ACTH over 24 h was reduced by 8% with 100 mg (P = 0.029) and by 8% with 200 mg (P = 0.018). The nadir concentration of ACTH over the 24 h and the ACTH concentration 24 h after sumatriptan were not, however, significantly reduced. All results are compared with placebo. 4 There was a reduction in the trough circulating cortisol concentration over 0-4 h which was 15% with 50 mg (P = 0.015), 14% with 100 mg (P = 0.022) and 24%with 200 mg (P < 0.001). The 5 h, post-prandial, peak cortisol concentration was reduced by 16% with 100 mg (P = 0.012) and by 15% with 200 mg (P = 0.017). The weighted mean cortisol over 24 h was reduced by 9% with 50 mg (P = 0.020), 9% by 100 mg (P = 0.024) and 12% by 200 mg (P = 0.002). The nadir concentration of cortisol over the 24 h and the cortisol concentration 24 h after the administration of sumatriptan were not, however, significantly reduced. All results are compared with placebo. 5 Sumatriptan did not inhibit the post-prandial peak in circulating concentrations of cortisol and ACTH, although there was a diminution of this peak following 100 mg and 200 mg relative to placebo. 6 There was no effect of sumatriptan on circulating ACTH and cortisol concentrations by 11 h after dosing, compared with placebo. 7 Sumatriptan has a small effect on the circulating cortisol concentration in healthy volunteers which is caused by a reduction in circulating ACTH concentration. These changes in hormone concentrations are within the normal diurnal variation and are not clinically important, even at twice the recommended therapeutic dose of 100 mg.

show abstract

The Corticotropin-Releasing Factor Release in Rat Hypophysial Portal Blood Is Mediated by Brain Catecholamines

Cited by 118 publications

References 16 publications

Insulin-induced hypoglycemia stimulates corticotropin-releasing factor and arginine vasopressin secretion into hypophysial portal blood of conscious, unrestrained rams.

Insulin-induced hypoglycemia stimulates corticotropin-releasing factor and arginine vasopressin secretion into hypophysial portal blood of conscious, unrestrained rams.

Divergent projections of catecholaminergic neurons in the nucleus of the solitary tract to limbic forebrain and medullary autonomic brain regions

The effects of oral sumatriptan, a 5‐HT1 receptor agonist, on circulating ACTH and cortisol concentrations in man.

Contact Info

Product

Resources

About