Adenosine A1 receptor-mediated inhibition of in vitro prolactin secretion from the rat anterior pituitary

Bibliographic Details
Title: Adenosine A1 receptor-mediated inhibition of in vitro prolactin secretion from the rat anterior pituitary
Authors: Picanço-Diniz, D.L.W., Valença, M.M., Antunes-Rodrigues, J.
Source: Brazilian Journal of Medical and Biological Research. November 2006 39(11)
Publisher Information: Associação Brasileira de Divulgação Científica, 2006.
Publication Year: 2006
Subject Terms: Cyclopentyltheophylline, Dibutyryl cAMP, R-PIA, Pertussis toxin, Cholera toxin
More Details: In previous studies, we demonstrated biphasic purinergic effects on prolactin (PRL) secretion stimulated by an adenosine A2 agonist. In the present study, we investigated the role of the activation of adenosine A1 receptors by (R)-N6-(2-phenylisopropyl)adenosine (R-PIA) at the pituitary level in in vitro PRL secretion. Hemipituitaries (one per cuvette in five replicates) from adult male rats were incubated. Administration of R-PIA (0.001, 0.01, 0.1, 1, and 10 µM) induced a reduction of PRL secretion into the medium in a U-shaped dose-response curve. The maximal reduction was obtained with 0.1 µM R-PIA (mean ± SEM, 36.01 ± 5.53 ng/mg tissue weight (t.w.)) treatment compared to control (264.56 ± 15.46 ng/mg t.w.). R-PIA inhibition (0.01 µM = 141.97 ± 15.79 vs control = 244.77 ± 13.79 ng/mg t.w.) of PRL release was blocked by 1 µM cyclopentyltheophylline, a specific A1 receptor antagonist (1 µM = 212.360 ± 26.560 ng/mg t.w.), whereas cyclopentyltheophylline alone (0.01, 0.1, 1 µM) had no effect. R-PIA (0.001, 0.01, 0.1, 1 µM) produced inhibition of PRL secretion stimulated by both phospholipase C (0.5 IU/mL; 977.44 ± 76.17 ng/mg t.w.) and dibutyryl cAMP (1 mM; 415.93 ± 37.66 ng/mg t.w.) with nadir established at the dose of 0.1 µM (225.55 ± 71.42 and 201.9 ± 19.08 ng/mg t.w., respectively). Similarly, R-PIA (0.01 µM) decreased (242.00 ± 24.00 ng/mg t.w.) the PRL secretion stimulated by cholera toxin (0.5 mg/mL; 1050.00 ± 70.00 ng/mg t.w.). In contrast, R-PIA had no effect (468.00 ± 34.00 ng/mg t.w.) on PRL secretion stimulation by pertussis toxin (0.5 mg/mL; 430.00 ± 26.00 ng/mg t.w.). These results suggest that inhibition of PRL secretion after A1 receptor activation by R-PIA is mediated by a Gi protein-dependent mechanism.
Document Type: article
File Description: text/html
Language: English
ISSN: 0100-879X
Access URL: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2006001100013
Rights: info:eu-repo/semantics/openAccess
Accession Number: edssci.S0100.879X2006001100013
Database: SciELO