Central Actions of Adenosine on Pituitary Secretion of Prolactin, Luteinizing Hormone and Thyrotropin

Jg, Ondo; Mw, Walker; Dd, Wheeler

doi:10.1159/000125183

Cited by 9 publications

(6 citation statements)

References 13 publications

(16 reference statements)

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“…The failure of rolipram to increase ir‐LH release suggests that mechanisms other than PDE‐4 inhibition may mediate the increases in LH release produced by denbufylline in vivo. An obvious possibility is blockade of adenosine A 1 receptors, although the apparent failure of an adenosine A 1 receptor agonist to influence serum ir‐LH when injected into the lateral ventricle (Ondo et al , 1989) does not accord with this view; nor does the inability of BRL 61063 to augment the secretion of the gonadotrophin.…”

Section: Discussionmentioning

confidence: 99%

Stimulation of the hypothalamo‐pituitary‐adrenal axis in the rat by three selective type‐4 phosphodiesterase inhibitors: in vitro and in vivo studies

Kumari

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Poyser

et al. 1997

British J Pharmacology

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1 Previous studies in our laboratory have shown that the synthetic xanthine analogue denbufylline, a selective type 4 phosphodiesterase (PDE-4) inhibitor, is a potent activator of the hypothalamo-pituitaryadrenal (HPA) axis when given orally or intraperitoneally (i.p.) to adult male rats. This paper describes the results of experiments in which well established in vivo and in vitro methods were used to compare the e ects of denbufylline on HPA function with those of two other selective PDE-4 inhibitors, rolipram and BRL 61063 (1,3-dicyclopropylmethyl-8-amino-xanthine 71 , i.c.v.) was also ine ective in this regard although at a higher dose (1 mg kg 71 , i.c.v.) it produced a small but signi®cant (P50.05) increase in ircorticosterone release. Denbufylline also increased the serum ir-LH concentration when given peripherally (0.2 ± 0.6 mg kg 71 , i.p., P50.05) or centrally (100 ng kg 71 , i.c.v., P50.05) but rolipram (1.6 ± 200 mg kg 71 , i.p. or 8 ng ± 1 mg kg 71 , i.c.v.) and BRL 61063 (0.25 ± 30 mg kg 71 , i.p. or 1 ng ± 1 mg kg 71 , i.c.v.) did not (P40.05). 3 In vitro rolipram (10 mM, P50.01), denbufylline (1 mM, P50.001) and BRL 61063 (1 and 10 mM, P50.05) stimulated the release of corticotrophin releasing hormone (ir-CRH-41) but lower concentrations of the drugs were without e ect as also was BRL 61063 at 100 mM (P40.05); the rank order of potency was thus BRL 610634rolipram4denbufylline. The adenylyl cyclase activator forskolin (100 mM, P50.01) also stimulated the release of ir-CRH-41, producing e ects which were additive with those of rolipram and denbufylline but not with those of BRL 61063. The secretory responses to forskolin (100 mM) were accompanied by a highly signi®cant increase in the cyclic AMP content of the hypothalamic tissue (P50.005). Rolipram (10 mM) also signi®cantly (P50.05) elevated the hypothalamic cyclic AMP but denbufylline (10 mM) and BRL 61063 (10 mM) did not. However, all three PDEinhibitors potentiated the rise in cyclic AMP induced by forskolin (P50.05). None of the drugs tested, alone or in combination, modi®ed the release of arginine vasopressin (ir-AVP) from the hypothalamus. 4 Rolipram (100 mM), denbufylline (100 mM) and BRL 61063 (100 mM) stimulated the release of corticotrophin (ir-ACTH) from pituitary tissue in vitro (P50.05) but in lower concentrations they were without signi®cant e ect. In addition, rolipram (10 mM, P50.05), denbufylline (0.1 mM, P50.05) and BRL 61063 (10 mM, P50.05) potentiated the signi®cant (P50.05) rises in ir-ACTH secretion induced by forskolin (100 mM). Forskolin (100 mM) also produced a highly signi®cant increase (P50.01) in the tissue cyclic AMP content which was further potentiated by rolipram (10 mM), denbufylline (10 mM) and BRL 61063 (10 mM) which, alone did not a ect the cyclic AMP content of the tissue. 5 Since both denbufylline and BRL 61063 possess signi®cant adenosine A 1 receptor blocking activity, further studies examined the potential in¯uence of these receptors on the secretion in vitro of CRH-41, AVP and ACTH. The release of ir-CR...

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Section: Discussionmentioning

confidence: 99%

Stimulation of the hypothalamo‐pituitary‐adrenal axis in the rat by three selective type‐4 phosphodiesterase inhibitors: in vitro and in vivo studies

Kumari

Cover

Poyser

et al. 1997

British J Pharmacology

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“…Adenosine has been reported to inhibit prolactin and growth hormone secretion from clonal pituitary cell lines (Dorflinger & Schonbrunn, 1985;Delahunty et al 1988), and either to stimulate or to inhibit the release of adrenocorticotrophic hormone from cultured an¬ terior pituitary cells (Anand-Srivastava et al 1989). Adenosine and adenosine analogues have also been reported to stimulate prolactin and luteinizing hormone release in vivo (Ondo et al 1989), while little (Ondo et al 1989) or no (Di Renzo et al 1990) effect has been described on the 'in-vivo' secretion of thyroid-stimulating hormone.…”

Section: Introductionmentioning

confidence: 99%

Direct effect of adenosine on prolactin secretion at the level of the single rat lactotroph: involvement of pertussis toxin-sensitive and -insensitive transducing mechanisms

Scorziello

Landolfi

Grimaldi

et al. 1993

Journal of Molecular Endocrinology

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We studied the effect of adenosine on prolactin secretion by the anterior pituitary, and the transduction mechanisms whereby the purine exerts its action. Adenosine inhibited prolactin release in basal and in vasoactive intestinal peptide (VIP)- or TRH-stimulated conditions. Pertussis toxin pretreatment reduced the inhibition of VIP-stimulated prolactin secretion which was induced by adenosine, while it completely abolished the effect of the purine on TRH-evoked prolactin release. In membrane preparations of anterior pituitary cells, adenosine reduced the adenylate cyclase activity stimulated by VIP. Such an inhibition was not blocked by pertussis toxin pretreatment. Furthermore, the purine reduced TRH-stimulated inositol phosphate production in cultured anterior pituitary cells, an effect that was reversed by pretreatment with pertussis toxin. In addition, the nucleoside did not significantly affect the TRH-induced rise in intracellular calcium. In conclusion, our data show that adenosine inhibits prolactin secretion, acting on purinergic receptors coupled to the adenylate cyclase enzyme and phospholipase C. The effect of the nucleoside on adenylate cyclase seems to be achieved either by the involvement of an adenosine receptor coupled to the catalytic subunit of the enzyme via a pertussis toxin-sensitive G protein, or by the activation of a site directly coupled to the catalytic subunit of the adenylate cyclase (the P site). Its effect on phospholipase C seems to be mediated by a purinergic receptor coupled to the intracellular effector via a pertussis toxin-sensitive G protein.

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“…A number of authors have shown that peripheral [67] or central [68] administration of adenosine can stimulate the release of PRL but not LH [68] or TSH [69]. These data, however, gave little insight into the site or mode of action of adenosine in the neuroendocrine system, and could in fact represent non-specific stressful actions.…”

Section: Biological Effects Of Purines In the Pituitary Gland Effectsmentioning

confidence: 99%

Novel insights into how purines regulate pituitary cell function

2003

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Purine nucleosides and nucleotides are widely distributed substances that exhibit a diverse range of effects in a number of tissues, acting as important extracellular signalling molecules in addition to their more established roles in cellular metabolism. They mediate their effects via activation of distinct cell surface receptors, termed adenosine (or P1) and P2 purinergic receptors. Although roles for adenosine and adenine nucleotides have been described previously in the pituitary gland, the distribution of the receptor subtypes and the effects of their activation on pituitary function are not well defined. Recent evidence, however, has emerged to describe a complex signalling system for purines in the pituitary gland. Data from a variety of studies have shown that the expression pattern, number and affinity of adenosine and/or P2 receptors may be cell-type specific and that non-endocrine in addition to endocrine cells elaborate these receptors. These variations, along with the diverse range of signalling pathways activated, dictate the response of individual cell types to extracellular purines, with roles now emerging for these substances in the regulation of hormone release, pituitary cell proliferation and cytokine/growth factor expression. In this review, we discuss these advances and examine some implications for pituitary growth control and the response of the hypothalamic-pituitary-adrenal axis to stress and inflammation.

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Central Actions of Adenosine on Pituitary Secretion of Prolactin, Luteinizing Hormone and Thyrotropin

Cited by 9 publications

References 13 publications

Stimulation of the hypothalamo‐pituitary‐adrenal axis in the rat by three selective type‐4 phosphodiesterase inhibitors: in vitro and in vivo studies

Stimulation of the hypothalamo‐pituitary‐adrenal axis in the rat by three selective type‐4 phosphodiesterase inhibitors: in vitro and in vivo studies

Direct effect of adenosine on prolactin secretion at the level of the single rat lactotroph: involvement of pertussis toxin-sensitive and -insensitive transducing mechanisms

Novel insights into how purines regulate pituitary cell function

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