Corticotropin-Releasing Factor-Like Immunoreactivity, Arginine Vasopressin-Like Immunoreactivity and ACTH-Releasing Bioactivity in Hypothalamic Tissue from Fetal and Neonatal Sheep

Brieu, V.; Tonon, Marie‐Christine; Lutz-Bucher, B.; Durand, Philippe

doi:10.1159/000125109

Cited by 25 publications

(7 citation statements)

References 13 publications

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“…Similarly, ex¬ periments using anesthetized rats (3) and conscious sheep (4,5) have demonstrated that concentrations of CRH and AVP in pituitary portal blood increase in response to stress stimuli. The source of these neuropeptide hormones in the rat is the hypophysiotropic CRH neurons originating in the parvocellular part of the hypothalamic paraventricular nucleus (6) and similar neurosecretory pathways are probably also involved in the sheep (7)(8)(9).In addition to these endogenous systems control¬ ling ACTH release, it is well established that exo¬ genous CRH and AVP will stimulate the pituitary/ adrenocortical axis directly in man and synergistic effects of these hormones on ACTH release have also been demonstrated in sheep (10-13). Also, however, studies have been carried out in man where CRH has been given to individuals in whom the release of AVP has been experimentally stimu¬ lated.…”

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confidence: 99%

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Dehydration, but not vasopressin infusion, enhances the adrenocortical responses of sheep to corticotropin-releasing hormone or restraint

Matthews¹,

Parrott²

1991

Acta Endocrinologica

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Two experiments were carried out using adult castrated sheep prepared with jugular vein catheters. In Experiment 1, sheep (N=8) were injected iv with saline vehicle, vehicle + 15 or 30 \g=m\g oCRH, or subjected to 120 min mild physical stress (restraint), following a 48 h period during which water was freely available or withheld. Blood samples were taken for 30 min before and 120 min after oCRH injection, and before and during restraint, and the plasma analysed for AVP and cortisol content. Levels of AVP increased by over 500% after dehydration, but were unaffected by oCRH or restraint. In contrast, plasma cortisol was unchanged after dehydration, but increased after oCRH and restraint. Moreover, these cortisol responses were significantly greater when the sheep were dehydrated. In Experiment 2, euhydrated sheep (N =6) were infused iv with saline vehicle or vehicle + AVP for a 5-h pretreatment period, followed by a 2-h experimental period in which the animals were injected with 15 \g=m\g oCRH or subjected to 120 min restraint, as in Experiment 1. Blood samples were taken throughout the experiment from a contralateral catheter and the plasma analysed for AVP and cortisol content. The AVP infusion produced plasma levels of the hormone approximately twice those seen after 48 h dehydration in Experiment 1, but did not affect cortisol secretion. Furthermore, the cortisol response to oCRH, or restraint, was not enhanced by the AVP infusion. These results suggest that pituitary responsiveness to exogenous or endogenous CRH (restraint stress) may be enhanced in sheep by dehydration through a mechanism that does not involve an adrenal or pituitary action of circulating AVP.In vitro studies have shown that both CRH and AVP are able to stimulate the secretion of ACTH in preparations of pituitary cells (1,2). Similarly, ex¬ periments using anesthetized rats (3) and conscious sheep (4,5) have demonstrated that concentrations of CRH and AVP in pituitary portal blood increase in response to stress stimuli. The source of these neuropeptide hormones in the rat is the hypophysiotropic CRH neurons originating in the parvocellular part of the hypothalamic paraventricular nucleus (6) and similar neurosecretory pathways are probably also involved in the sheep (7)(8)(9).In addition to these endogenous systems control¬ ling ACTH release, it is well established that exo¬ genous CRH and AVP will stimulate the pituitary/ adrenocortical axis directly in man and synergistic effects of these hormones on ACTH release have also been demonstrated in sheep (10-13). Also, however, studies have been carried out in man where CRH has been given to individuals in whom the release of AVP has been experimentally stimu¬ lated. These investigations have shown that in¬ creasing neurohypophysial AVP secretion by hypertonic saline infusion (14-16), or dehydration (17), enhances the pituitary-adrenocortical re¬ sponse to CRH. Thus, the pituitary effects of exo¬ genous CRH seem to be facilitated under condi¬ tions where the neurosecretory activity of magnocel...

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confidence: 99%

mentioning

confidence: 99%

Dehydration, but not vasopressin infusion, enhances the adrenocortical responses of sheep to corticotropin-releasing hormone or restraint

Matthews¹,

Parrott²

1991

Acta Endocrinologica

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“…There is a clear developmental influence on its secretion in response to hypotension during fetal life in the sheep (1). Also, AVP is present very early in fetal life (10,11) and appears important in the stimulation of ACTH secretion. Its relationship to the appearance of corticotrophin-releasing factor and its function in the stimulation of ACTH secretion change with development in both the sheep (10) and the rat (11).…”

Section: Discussionmentioning

confidence: 99%

“…It is likely that the pituitary portal levels of AVP were elevated in the fetus, resulting in the secretion of ACTH. Brieu et al (10) concluded that AVP is more important in the stimulation of ACTH secretion in fetuses younger than 138 d gestation than at term, with corticotropin-releasing factor assuming a progressively more important role. The fetal cortisol response and its absence in the neonates reflects this ontogenetic phenomenon.…”

Section: Discussionmentioning

confidence: 99%

Central α-1-Adrenergic Control of Vasopressin Secretion in Newborn Lambs

1991

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ABSTRACT. The hypothesis that central a-1 adrenoceptors are inhibitory to the hypotension-induced secretion of vasopressin was tested by subjecting lambs that were instrumented for a long term to varying degrees of hypotension after intracerebroventricular injections of prazosin or placebo. Eight lambs in the 1st wk of life treated with intracerebroventricular injections of placebo had their mean arterial blood pressures decreased 14 and 21% by i.v. infusion of nitroprusside. Arginine vasopressin levels rose to 7.3 1 2.4 pmol/L only with the greater degree of hypotension. When the lambs were treated with intracerebroventricular injections of 1 pg/kg of prazosin, the blood pressures were decreased 13 and 23%, and the vasopressin levels were 15.4 2 16.6 and 27.5 2 20.3 pmol/L, respectively. A relationship was shown between the degree of hypotension and the plasma arginine vasopressin levels with both the placebo and prazosin, the slope being much steeper for the prazosin treatment (-1.11) than for the placebo treatment (-0.31). Plasma renin activity was increased a similar amount in both groups, and there was no change in plasma cortisol levels. We conclude that a-1 adrenoceptors in the brain are inhibitory to the secretion of arginine vasopressin. These results differ from observationsh adult rats and dogs and may be accounted for by developmental or species differences. (Pediatr Res 30: 50-54,1991) Abbreviations AVP, arginine vasopressin CSF, cerebrospinal fluid HR, heart rate ICV, intracerebroventricular MABP, mean arterial blood pressure PE, phenylephrine PRA, plasma renin activity AVP has been shown to have a role in fetal and neonatal cardiovascular homeostasis as a "stress" hormone (1-3). Neonatal and fetal AVP secretion may be induced by hypoxia, hypotension, and acidosis. Levels of this hormone are particularly high around the time of delivery, especially in the case of fetal asphyxia (3).Although there is an increasing body of knowledge concerning the control of AVP secretion in adult animals, little is known about the neonate. CNS a-1 and a-2 adrenoceptors are involved in the regulation of AVP secretion in adult animals (4-6). We have previously reported that lamb fetuses treated with i.v. prazosin, an a-1 adrenoceptor blocker, and subsequently subjected to hypotensive hemorrhage had excessive levels of AVP when compared with similar hemorrhagic hypotension without prazosin (7). This observation led us to hypothesize that hypothalamic a-1 receptors exert an inhibitory influence on the secretion of AVP in response to hypotension in the near-term lamb fetus. In the neonatal lamb, AVP levels after hemorrhage were similar with prazosin and with vehicle, but the relative decrease in blood pressure was less in the prazosin-treated lambs and may have been subthreshold for the secretion of AVP (2). To prove our hypothesis, we designed an experiment in which CNS a-1 adrenoceptor blockade was achieved in the newborn lamb by ICV injection, rather than i.v. injection of prazosin. In so doing, we hoped to avoid t...

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“…This normal pattern can be delayed by foetal adrenalectomy, and accelerated by infusion of cortisol into the foetus (Antolovich et al 1988). When cortisol was added to foetal pituitary cells in vitro there was an increase in the ratio of bioactive to immunoreactive ACTH secreted into the culture medium (Brieu et al 1989). The suggestion has been made, therefore, that cortisol exerts a positive feed-forward effect at the level of the foetal pituitary during late gestation to promote changes in foetal pituitary corticotroph histology and to enhance secretion of a form of ACTH (presumably ACTH1-39), with greater biological activity.…”

Section: Activation Of Foetal Pituitary Functionmentioning

confidence: 99%

Foetal endocrine maturation

Challis

Bassett

Berdusco

et al. 1993

Equine Veterinary Journal

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In domestic ruminants such as the sheep, birth is effected through sequential maturation of the foetal hypothalamicpituitary-adrenal (HPA) axis, leading to the increased output of cortisol. Factors regulating foetal pituitary adrenocorticotrophin (ACTH) secretion have been delineated, and these include corticotrophin releasing hormone (CRH), arginine vasopressin, prostaglandin (PG) E2 and endogenous opioids. The pre-partum increase in foetal plasma ACTH is associated with a rise in pro-opiomelanocortin (POMC) mRNA in the foetal pars distalis, and with an altered pattern of POMC post-translational processing. Foetal adrenal activation results from an increase in ACTH receptors and enhanced coupling through the Gs protein to adenylate cyclase, and increased expression of key steroidogenic enzymes including P45OC1p Cortisol modulates the mechanism by which ACTH activates foetal adrenal function, through specific glucocorticoid receptors (GR) in the foetal adrenal cortex. Although the numbers of GR change with gestation, the relative abundance of GR mRNA does not, pointing to post-translational regulatory mechanisms. Cortisol also stimulates an increase in the concentration of its own high affinity binding protein (corticosteroid binding globulin; CBG) in the foetal circulation, apparently by increasing CBG gene expression in the foetal liver, and by altering the extent of foetal CBG glycosylation in a manner that would be expected to decrease the metabolic clearance of this glycoprotein. Clear evidence for placental CRH and ACTH production is lacking in sheep, but PGE2, produced in increasing amounts by the placenta during late pregnancy, may augment the drive to HPA maturation. Aspects of the maturational pathway of cortisol biosynthesis have been described in other species, including the horse, and some comparison is made with the more detailed information currently available from species such as the sheep.

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Corticotropin-Releasing Factor-Like Immunoreactivity, Arginine Vasopressin-Like Immunoreactivity and ACTH-Releasing Bioactivity in Hypothalamic Tissue from Fetal and Neonatal Sheep

Cited by 25 publications

References 13 publications

Dehydration, but not vasopressin infusion, enhances the adrenocortical responses of sheep to corticotropin-releasing hormone or restraint

Dehydration, but not vasopressin infusion, enhances the adrenocortical responses of sheep to corticotropin-releasing hormone or restraint

Central α-1-Adrenergic Control of Vasopressin Secretion in Newborn Lambs

Foetal endocrine maturation

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