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, Antonella; Landolfi, E.; Grimaldi, M.; Meucci, Olimpia; Ventra, C.; Avallone, Antonio; Postiglione, Alfredo; Schettini, Gennaro

doi:10.1677/jme.0.0110325

Cited by 12 publications

(20 citation statements)

References 25 publications

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“…(2)). This indicated the presence of A2 receptors and subsequent studies also showed the existence of A1 receptors that are coupled to adenylate cyclase and phospholipase C in several pituitary cell lines [105][106][107][108][109]. More detailed experiments using several complementary methods showed that adenosine receptors are differentially expressed in the different cell types within the anterior pituitary gland [110][111][112].…”

Section: Anterior Pituitary Glandmentioning

confidence: 81%

The Adenosine A2b Receptor: Its Role in Inflammation

Ham¹,

Rees²

2008

EMIDDT

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Investigations into the role of the adenosine A2b receptor have been enigmatic due to the lack of good selective high affinity agonists and antagonists. Over the last few years several new antagonist compounds, based either on a xanthine or pyrrolpyrimidine (polyheterocyclic) structure have been designed and these have been used to localise A2b receptors in different tissues and to determine their function. Recently, animals harbouring either a loss or an over-expression of the A2b receptor have been created and these suggest an anti-inflammatory role for the receptor. In this short review, we describe how the A2b receptor influences inflammation in different tissues. In the anterior pituitary gland the A2b receptors exist predominantly in folliculostellate cells where it stimulates secretion of IL-6 and VEGF and influences gap-junctional communication via connexin-43. The A2b receptor also mediates the release of pro-inflammatory cytokines from many tissues such as bronchial smooth muscle, intestinal epithelial cells and mast cells. The presence of a HIF-1alpha binding site in the promoter region of the A2b receptor gene shows that it is strongly implicated in hypoxia and angiogenesis. Targeting the A2b receptor may also be useful in combating autoimmune type I diabetes. These findings, together, indicate that the A2b receptor plays a role in inflammation; its precise action, whether pro- or anti-inflammatory however may be cell type dependent. Nevertheless several A2b receptor antagonists are being developed for therapeutic intervention and these are either at the preclinical stage or in phase I clinical trials as is the case for CVT-6883 for asthma.

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Section: Anterior Pituitary Glandmentioning

confidence: 81%

The Adenosine A2b Receptor: Its Role in Inflammation

Ham¹,

Rees²

2008

EMIDDT

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“…This negative coupling indicates the involvement of inhibitory G proteins, which are pertussis toxin-sensitive. More recently, Scorziello et al (1993) have demonstrated that the direct effect of adenosine on prolactin secretion in the rat lactotroph involves pertussis toxin-sensitive and -insensitive transducing mechanisms. Adenosine actions have also been studied in cells derived from rat pituitary tumors: GH3 and GH4 cells, which secrete prolactin and growth hormone.…”

mentioning

confidence: 99%

Regulation of L‐Type Calcium Channels in GH₄ Cells via A₁ Adenosine Receptors

Zapata

Navarro

Canela

et al. 1997

Journal of Neurochemistry

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Identification of A1 adenosine receptors (A1 Ps) in a tumor cell line derived from rat pituitary (GH4 ce~is) was performed by ligand binding and immunological experiments. Subsequently, the involvement of A1Rs in the regulation of calcium conductance was studied in these cells. The agonist N 6-(R) -(2-phenylisopropyl) adenosine (R-PIA) did not modify the intracellular calcium basal levels, whereas it inhibited the increase produced by 15mM KCI depolarization. The antagonist 1 ,3-dipropyl-8-cyclopentylxanthine led to the opening of voltage-dependent cell surface calcium channels in the absence of exogenous KCI. The channels were of the L type because the effect was abolished by calciseptine and by verapamil. These results suggest that endogenous adenosine exerts a tonic inhibitory effect on calcium transport. This was confirmed by the high adenosine concentration found in cell supernatants (up to 1 pM) and by the calcium mobilization produced by exogenously added adenosine deaminase. In depolarizing conditions, the calcium peak in the presence of adenosine deaminase was reduced when cells were preincubated with R-PIA, thus suggesting that A 1R activation regulates the intensity of depolarization. These results demonstrate that adenosine is an important regulator of the physiological state of pituitary tumor cells by modulating, in an autocrine manner, the activity of Ltype voltage-dependent calcium channels.

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“…Recent studies have demonstrated that adenosine inhibits prolactin secretion by acting on a purinergic receptor that modulates the activity of the enzymes adenyl cyclase and phospholipase C by a mechanism depending on membrane G i P activation (16). Other studies have shown that administration of R-PIA inhibits the release of PRL induced by TRH by inhibiting the decrease in phosphatidylinositol and cAMP synthesis in GH 3 cell lines (10).…”

Section: Discussionmentioning

confidence: 99%

Possible involvement of A1 receptors in the inhibition of gonadotropin secretion induced by adenosine in rat hemipituitaries in vitro

Picanço-Diniz

Valênça

Favaretto

et al. 1999

Braz J Med Biol Res

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We investigated the participation of A 1 or A 2 receptors in the gonadotrope and their role in the regulation of LH and FSH secretion in adult rat hemipituitary preparations, using adenosine analogues. A dosedependent inhibition of LH and FSH secretion was observed after the administration of graded doses of the R-isomer of phenylisopropyladenosine (R-PIA; 1 nM, 10 nM, 100 nM, 1 µM and 10 µM). The effect of R-PIA (10 nM) was blocked by the addition of 8-cyclopentyltheophylline (CPT), a selective A 1 adenosine receptor antagonist, at the dose of 1 µM. The addition of an A 2 receptor-specific agonist, 5-Nmethylcarboxamidoadenosine (MECA), at the doses of 1 nM to 1 µM had no significant effect on LH or FSH secretion, suggesting the absence of this receptor subtype in the gonadotrope. However, a sharp inhibition of the basal secretion of these gonadotropins was observed after the administration of 10 µM MECA. This effect mimicked the inhibition induced by R-PIA, supporting the hypothesis of the presence of A 1 receptors in the gonadotrope. R-PIA (1 nM to 1 µM) also inhibited the secretion of LH and FSH induced by phospholipase C (0.5 IU/ml) in a dose-dependent manner. These results suggest the presence of A 1 receptors and the absence of A 2 receptors in the gonadotrope. It is possible that the inhibition of LH and FSH secretion resulting from the activation of A 1 receptors may have occurred independently of the increase in membrane phosphoinositide synthesis.

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

Cited by 12 publications

References 25 publications

The Adenosine A2b Receptor: Its Role in Inflammation

The Adenosine A2b Receptor: Its Role in Inflammation

Regulation of L‐Type Calcium Channels in GH₄ Cells via A₁ Adenosine Receptors

Possible involvement of A1 receptors in the inhibition of gonadotropin secretion induced by adenosine in rat hemipituitaries in vitro

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

Cited by 12 publications

References 25 publications

The Adenosine A2b Receptor: Its Role in Inflammation

The Adenosine A2b Receptor: Its Role in Inflammation

Regulation of L‐Type Calcium Channels in GH4 Cells via A1 Adenosine Receptors

Possible involvement of A1 receptors in the inhibition of gonadotropin secretion induced by adenosine in rat hemipituitaries in vitro

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Regulation of L‐Type Calcium Channels in GH₄ Cells via A₁ Adenosine Receptors