Abstract
Adenosine has been implicated in various aspects of pituitary function but little is known of its role in the regulation of thyrotrophin (TSH) release. This study examined the effects of adenosine deaminase (ADA, which provokes adenosine breakdown) and selective adenosine-receptor ligands on the secretion of immunoreactive (ir-) TSH and prolactin (PRL) by rat anterior pituitary segments in vitro. ADA (5U/ml) stimulated the release of both hormones (P<0.01) as also did the selective adenosine A 1-receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 0.1 & 1nM, P<0.01); the responses to ADA were inhibited by an A 1-receptor agonist, N 6-cyclohexyladenosine (0.1-10nM, P<0.01). A non-selective A 1/A 2-receptor agonist, N-cyclopropylcarboxamidoadenosine (1–100nM) had mixed effects on ir-TSH release. However, the A 2A-receptor selective agonist, CGS 21680 (1-100nM) increased ir-TSH (P<0.05) and ir-PRL release (P<0.01); its effects on ir-TSH were blocked by concentrations of DPCPX (100nM, P<0.01) sufficient to antagonize A 2-receptors. These data suggest that adenosine acts via A 1-receptors to tonically suppress ir-PRL and ir-TSH release but that A 2A-receptor activation enhances the release of both hormones.
Published Version
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