Adrenergic Mechanisms Involved in the Control of Pituitary-Adrenal Activity in the Rat: A β-Adrenergic Stimulatory Mechanism

Tilders, F. J. H.; Berkenbosch, Frank; Smelik, P. G.

doi:10.1210/endo-110-1-114

Cited by 107 publications

(37 citation statements)

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“…Previous work has shown that catecholamines can elevate the levels of plasma ACTH (4,(12)(13)(14). The precise mechanism by which catecholamines can induce this effect has not been demonstrated.…”

Section: Discussionmentioning

confidence: 97%

“…Catecholamines also can induce the release of ACTH; however, it has not yet been established whether they act directly on the anterior pituitary or produce this effect indirectly by a central reflex mechanism (2). Peripheral administration of epinephrine increases plasma ACTH levels in rats (3)(4)(5). This increase is blocked by the 3-adrenergic receptor antagonist propranolol.…”

Section: -Adrenergic Receptorsmentioning

confidence: 99%

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Direct stimulation of beta 2-adrenergic receptors in rat anterior pituitary induces the release of adrenocorticotropin in vivo.

Mezey¹,

Reisine²,

Palkovits³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

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Previous work in our laboratory has shown that stimulation of g32-adrenergic receptors on mouse. anterior pituitary tumor cells causes the secretion of immunoreactive adrenocorticotropin (ACTH). The present study was designed to test the hypothesis that catecholamines can cause the release of ACTH in vivo by the direct stimulation of f32-adrenergic receptors in the rat anterior pituitary. Systemic administration of a 3-adrenergic receptor agonist (-)-isoproterenol resulted in an increase in plasma ACTH levels in intact animals and in rats with transected pituitary stalks. This effect could be blocked by the 8i-adrenergic receptor antagonist, propranolol, but not by the specific (31-adrenergic receptor antagonist, practolol. Salmefamol, a fi2-adrenergic receptor agonist also elevated plasma ACTH levels in stalk-sectioned animals. Dexamethasone, a Surgery. Two kinds of surgical interventions were performed. In one group of animals, the pituitary stalk was transected by means of a parapharyngeal approach. In another group of rats the median eminence was destroyed by means of a dorsal approach, with a small Hala'sz knife (8) (1.5-mm radius) that was lowered into the brain in the midline until it touched the ventral surface of the cranial vault and then moved in the midsagittal line from the bregma level to the mamillary bodies while being rotated continuously. In this way the median eminence and arcuate nuclei were destroyed. The results of the surgical procedures were verified at the time that the animals were killed.Injection Protocol. The following drugs were dissolved in 0.2 ml of saline and administered intraperitoneally: (-)-isoproterenol, 25 ug; d,l-propranolol, 500 Ag; practolol, 500 pug; salmefamol, 25 Ag; dexamethasone, 400 pug. Isoproterenol, salmefamol, and saline (control) were injected 30 min before killing the rats. Propranolol and practolol were given 40 min before the isoproterenol injection. Dexamethasone was injected 16 hr prior to administration of the other drugs.Plasma Collection. The animals were decapitated 5 see after being removed from their cages. After decapitation, trunk blood was collected in ice-cold polystyrene tubes containing 100 A.l of 10% EDTA. The blood was centrifuged at 3,000 x g for 20 min, and the plasma was removed, centrifuged again, and stored at -250C.Determination of ACTH. ACTH was extracted from the plasma as described by van Dijk (9). Blood (1.5 ml) was extracted with Vycor glass powder (35 mg per tube) from which the ACTH was eluted with 50% acetone. The extracts were dried in a vacuum centrifuge and reconstituted in veronal buffer (10). ACTH was determined by radioimmunoassay as described (10). To determine the ACTH recovery, internal standards were added to plasma of hypophysectomized rats and extracted and assayed as described above. All values are corrected for recovery, which was about 50%. A sample of pooled plasma was run with each radioimmunoassay to determine the interassay variation (15-18%). The immunoreactive ACTH detected by the radioimmunoassa...

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Section: Discussionmentioning

confidence: 97%

Section: -Adrenergic Receptorsmentioning

confidence: 99%

Direct stimulation of beta 2-adrenergic receptors in rat anterior pituitary induces the release of adrenocorticotropin in vivo.

Mezey¹,

Reisine²,

Palkovits³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

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“…Moreover, intracerebroventricular infusion of AVP and CRH increased plasma cortisol concentrations equally in equimolar concentrations in sheep [38,40]. Although these studies indicate that AVP and CRH could be major secretagogues to stimulate ACTH secretion in sheep, other factors such as catecholamines also play a role [25,35,36]. Moreover, the relative significance of AVP and CRH on the pituitary-adrenocortical system was reported to be stress-specific [3,26,29].…”

Section: Discussionmentioning

confidence: 99%

Effects of AVP V1a and CRH Receptor Antagonist on Psychological Stress Responses to Frustrating Condition in Sheep

Yayou

Nakamura

Ito

2009

The Journal of Veterinary Medical Science

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ABSTRACT. Arginine vasopressin (AVP) and corticotropin-releasing hormone (CRH) are released in the brain to regulate behavioral and physiological stress responses. To elucidate the respective roles of these peptides under certain stressors, we examined the effects of intracerebroventricular infusions of either AVP V1a receptor antagonist, [Pmp 1 , Tyr (Me) 2 ]-Arg 8 -Vasopressin (Pmp, Tyr-AVP) or CRH receptor antagonist, alpha-helical CRF 9-41 (hCRF) on stress responses induced by frustrating condition in sheep. Four ovariectomized Corriedale ewes were assigned to the experiment. In a "frustrating" condition (FC), food was withheld for 60 minutes from only the experimental ewe while this ewe was in the presence of the other ewes that were given food. As "non-frustrating" control condition (C), food was withheld for 60 minutes from all ewes, thereby controlling for the nonspecific effects of lack of food. FC induced a significant rise in the plasma cortisol concentration (p < 0.05) and increased the pawing number and rectal temperature compared with that in C (p < 0.1). The effects of either Pmp, Tyr-AVP or hCRF on these stress responses were analyzed. The rise in cortisol restored nearly to the control level by infusion of Pmp, Tyr-AVP or hCRF. The pawing number restored nearly to the control level by hCRF. The hyperthermia restored nearly to the control level by Pmp, Tyr-AVP. These data suggest that both endogenous CRH and AVP might be concerned with inducing physiological and behavioral stress responses to frustrating condition in sheep. KEY WORDS: arginine vasopressin V1a receptor antagonist, frustration, hyperthermia, hypothalamo-pituitary-adrenal axis, ovine corticotropin-releasing hormone antagonist.J. Vet. Med. Sci. 71(4): [431][432][433][434][435][436][437][438][439] 2009 Neuropeptides arginine vasopressin (AVP) and corticotropin-releasing hormone (CRH) are released in the hypothalamus, amygdala, and lateral septum during stress to regulate behavioral and physiological stress responses in rats and mice [9,19]. We previously reported the central effects of intracerebroventricular infusions of AVP and CRH in sheep [38,40]. Centrally infused CRH had equal potential to release cortisol into the systemic circulation as AVP [38,40], although many studies confirm that adrenocorticotropic hormone (ACTH) release is under the predominant control of AVP in sheep [10,11,31]. Centrally infused AVP also induced several types of stress-related behaviors, such as oral stereotyped behaviors [40], whereas CRH induced only stereotypical bleating [38]. Neither CRH nor AVP had an effect on autonomic nervous function, such as heart rate (HR) and rectal temperature (RT) [38,40]. Although we had showed that intracerebroventricular infusions of CRH and AVP could partly mimic the adrenocortical and behavioral stress responses, there was no context or environmental challenge such as anxiety-eliciting or stressrelated stimuli. To confirm the roles of CRH and AVP in regulating endocrine, behavioral, and autonomic stress respo...

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“…Adrenocorticotropin (ACTH) release is stimulated by a variety of hormones including corticotropin-releasing factor (CRF) (1,2), vasopressin (3,4), and catecholamines (5). These hormones may evoke secretion by initiating multiple events within the corticotroph.…”

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confidence: 99%

Corticotropin-releasing factor-induced adrenocorticotropin hormone release and synthesis is blocked by incorporation of the inhibitor of cyclic AMP-dependent protein kinase into anterior pituitary tumor cells by liposomes.

Reisine¹,

Rougon²,

Barbet³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

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Corticotropin-relessing factor (CRF) is the most potent and effective natural stimulant of corticotropin (ACTH) secretion. In a tumor cell line of the mouse anterior pituitary (AtT-20/D16-16) consisting of a homogenous population of corticotrophs, CRF is known to increase adenylate cyclase and cAMP-dependent protein kinase activities as well as to release ACTH. To determine whether activation of cAMPdependent protein kinase is essential for CRF to evoke the secretion of ACTH, an inhibitor (PKI) of this kinase was inserted into AtT-20 cells. This was accomplished by frtst encapsulating PKI into liposomes and then covalently coupling them to protein A for binding to antibodies directed against an AtT-20 cell surface antigen, N-CAM (neural cell adhesion molecule). The binding of the liposomes to the anti-N-CAM antibodies led to the internalization of the PKI into the tumor cells. The PKI treatment greatly attenuated CRF-stimulated ACTH release as well as the secretory response to ,-adrenergic agonists. However, ACTH release in response to caerulein, an agonist of cholecystokinin 8 receptors, was not altered by the PKI treatment. CRF treatment also increased the levels of mRNA for proopiomelanocortin (POMC), the precursor for ACTH in AtT-20 cells. Application ofliposomes containing PKI to AtT-20 cells blocked the ability of CRF and 8-bromo-cAMP, but not phorbol ester, to increase POMC mRNA levels. The results revealed an essential role for cAMP in mediating the effect of CRF on ACTH release and POMC gene expression.Adrenocorticotropin (ACTH) release is stimulated by a variety of hormones including corticotropin-releasing factor (CRF) (1, 2), vasopressin (3,4), and catecholamines (5). These hormones may evoke secretion by initiating multiple events within the corticotroph. CRF activates both adenylate cyclase and cAMP-dependent protein kinase in rat anterior pituitary membranes (6) and homogenates of a tumor cell line of the mouse anterior pituitary (AtT-20/D16-16) consisting of a homogenous population of corticotrophs (7,8). These data suggest that cAMP is involved in the receptor-mediated release of ACTH. 8-Adrenergic agonists, which stimulate cAMP-dependent protein kinase activity and the secretion of ACTH from AtT-20 cells (7), also depolarize AtT-20 cells and increase the frequency of action potentials in these corticotrophs (9, 10). This electrical activity has been associated with transient calcium currents (9, 10), and (3-adrenergic agonists and forskolin, a direct activator at adenylate cyclase, increase cytosolic calcium levels in . In addition to cAMP and calcium, activators of protein kinase C evoke ACTH release (12), and recent studies (13) have suggested a role for phosphatidylinositol turnover in hormone secretion from corticotrophs.

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Adrenergic Mechanisms Involved in the Control of Pituitary-Adrenal Activity in the Rat: A β-Adrenergic Stimulatory Mechanism

Cited by 107 publications

References 0 publications

Direct stimulation of beta 2-adrenergic receptors in rat anterior pituitary induces the release of adrenocorticotropin in vivo.

Direct stimulation of beta 2-adrenergic receptors in rat anterior pituitary induces the release of adrenocorticotropin in vivo.

Effects of AVP V1a and CRH Receptor Antagonist on Psychological Stress Responses to Frustrating Condition in Sheep

Corticotropin-releasing factor-induced adrenocorticotropin hormone release and synthesis is blocked by incorporation of the inhibitor of cyclic AMP-dependent protein kinase into anterior pituitary tumor cells by liposomes.

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