Monophasic displacement of [125I]-GTNH2 from 5-HT1d binding sites

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 A1-receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 0.1 & 1nM, P<0.01); the responses to ADA were inhibited by an A1-receptor agonist, N6-cyclohexyladenosine (0.1-10nM, P<0.01). A non-selective A1/A2-receptor agonist, N-cyclopropylcarboxamidoadenosine (1–100nM) had mixed effects on ir-TSH release. However, the A2A-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 A2-receptors. These data suggest that adenosine acts via A1-receptors to tonically suppress ir-PRL and ir-TSH release but that A2A-receptor activation enhances the release of both hormones.