Effects of pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal polypeptide on cyclic AMP accumulation in sheep pituitary cells in vitro

Sawangjaroen, Kitja; Sernia, Conrad; Curlewis, J. D.

doi:10.1677/joe.0.1480545

Cited by 8 publications

(1 citation statement)

References 30 publications

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“…Pituitary glands from sexually mature merino ewes of unknown age were dispersed by incubation with trypsin as previously described in detail ( 12, 13). Dispersed cells were plated into 24‐well plates at a density of 500 000 cells/well and were preincubated for 3 days in Foetal Calf Serum‐supplemented Dulbecco’s modification of Eagle’s medium (DMEM) before use.…”

Section: Methodsmentioning

confidence: 99%

Adrenoceptor Subtype Involvement in Suppression of Prolactin Secretion by Noradrenaline

Colthorpe

Nalliah

Anderson

et al. 2000

J Neuroendocrinology

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In sheep, injection of noradrenaline suppresses prolactin secretion by a direct effect at the pituitary gland. The aims of this study were to use primary cultures of ovine pituitary cells to examine the receptor subtypes that mediate the inhibitory effect of noradrenaline on prolactin secretion and, by using receptor antagonists in vivo, determine whether noradrenaline acts as a prolactin release-inhibiting factor (PIF). Noradrenaline and dopamine suppressed prolactin secretion from ovine pituitary cells with ED50s of 60.9+/-46.6 and 1.5+/-1.0x10-9 mol/l, respectively (P<0.05). The in-vitro prolactin release-inhibiting effect of noradrenaline (10-7 mol/l) was not blocked by the dopamine antagonists pimozide (D2) or SCH23390 (D1) but was blocked by each of the adrenoceptor antagonists (alpha1-adrenoceptor antagonists prazosin and WB4101, the alpha2-adrenoceptor antagonist yohimbine and the beta-adrenoceptor antagonist propranolol). The response to adrenoceptor agonists was also tested in vitro. The alpha1-adrenoceptor agonists phenylephrine and cirazoline significantly suppressed prolactin. Of the alpha2-agonists, clonidine had no effect whereas oxymetazoline and p-aminoclonidine both suppressed prolactin. The beta-adrenoceptor agonist isoproterenol also suppressed prolactin while the specific beta3-antagonist BRL37344 had no effect. When the adrenoceptor antagonists were tested in vivo in ewes manipulated to be in the luteal phase, only WB4101 significantly (P<0.05) increased plasma prolactin concentrations but this response was small and only observed in one of two experiments. In summary, these experiments suggest that adrenoceptors and not dopamine receptors are responsible for the inhibitory effect of noradrenaline on prolactin secretion in vitro but do not implicate a particular adrenoceptor subtype. The in-vivo experiments do not provide convincing evidence for a role for noradrenaline as a physiologically important PIF.

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Section: Methodsmentioning

confidence: 99%

Adrenoceptor Subtype Involvement in Suppression of Prolactin Secretion by Noradrenaline

Colthorpe

Nalliah

Anderson

et al. 2000

J Neuroendocrinology

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PACAP stimulates dopamine neuronal activity in the medial basal hypothalamus and inhibits prolactin

Anderson

Curlewis

1998

Brain Research

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Enhanced reactivity of the adrenal medulla in response to pituitary adenylate cyclase activating polypeptide<sub>1-27</sub> (PACAP) during insulin-induced hypoglycemia in anesthetized dogs

Yamaguchi

1999

Rev. can. physiol. pharmacol.

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The present study was to test the hypothesis that the reactivity of the adrenal medulla to pituitary adenylate cyclase activating polypeptide1-27 (PACAP27) is enhanced during insulin-induced hypoglycemia (IIH) in anesthetized dogs. Plasma catecholamine (CA) concentrations in adrenal venous and aortic blood were determined by an HPLC method coupled with electrochemical detection, and the plasma glucose concentration in aortic blood was measured using a glucometer. PACAP27 (25 ng) was administered locally via the adrenolumbar artery to the left adrenal gland. The resulting CA responses were compared before and during IIH following an intravenous bolus injection of insulin (0.15 IU/kg, i.v.). In the first group with normal adrenal innervation, the basal adrenal CA secretion gradually increased, reaching a maximum level 45 min after the insulin injection. The net increase in PACAP27-induced CA secretion was significantly greater 30, 45, and 60 min after the induction of hypoglycemia, compared with the initial net response to PACAP27 observed before insulin injection. In the second group receiving local adrenal denervation, neither the basal CA secretion nor the net CA response to PACAP27 significantly increased despite the presence of IIH, which developed to an extent similar to that found in the first group. In the third group, which was the normoglycemic control group, both the basal CA secretion and the net CA response to PACAP27 remained unchanged during the experimental period. The results indicate that the adrenomedullary reactivity to PACAP27 was significantly enhanced during IIH only when the sympathoadrenal system was activated. The present study suggests that PACAP27 may play a beneficial role in glucose counterregulatory mechanisms in the adrenal medulla during hypoglycemia.

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Effects of pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal polypeptide on cyclic AMP accumulation in sheep pituitary cells in vitro

Cited by 8 publications

References 30 publications

Adrenoceptor Subtype Involvement in Suppression of Prolactin Secretion by Noradrenaline

Adrenoceptor Subtype Involvement in Suppression of Prolactin Secretion by Noradrenaline

PACAP stimulates dopamine neuronal activity in the medial basal hypothalamus and inhibits prolactin

Enhanced reactivity of the adrenal medulla in response to pituitary adenylate cyclase activating polypeptide<sub>1-27</sub> (PACAP) during insulin-induced hypoglycemia in anesthetized dogs

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