Please use this identifier to cite or link to this item: http://repositorio.ufpa.br/jspui/handle/2011/3291
Compartilhar:
Type: Artigo de Periódico
Issue Date: Nov-2006
Authors: DINIZ, Domingos Luiz Wanderley Picanço
VALENÇA, Marcelo Moraes
RODRIGUES, José Antunes
Title: Adenosine A1 receptor-mediated inhibition of in vitro prolactin secretion from the rat anterior pituitary
Citation: PICANÇO-DINIZ, D.L.W.; VALENÇA, M.M.; ANTUNES-RODRIGUES, J. Adenosine A1 receptor-mediated inhibition of in vitro prolactin secretion from the rat anterior pituitary. Brazilian Journal of Medical and Biological Research, Ribeirão Preto, v. 39, n. 11, p. 1493-1499, nov. 2006. Disponível em: <http://www.scielo.br/pdf/bjmbr/v39n11/6262.pdf>. Acesso em: 11 dez. 2012.
Abstract: 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.
Keywords: Dibutiril
CAMP
Teofilina ciclopentilo
Colera toxina
Pertussis toxina
ISSN: 1414-431X
metadata.dc.rights: Acesso Aberto
Appears in Collections:Artigos Científicos - ICB

Files in This Item:
File Description SizeFormat 
Artigo_AdenosineReceptorMediated.pdf495.86 kBAdobe PDFView/Open


This item is licensed under a Creative Commons License Creative Commons