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Adenosine A1 receptor-mediated inhibition of in vitro prolactin secretion from the rat anterior pituitary
Picanço-Diniz, D. L. W; Valença, M. M; Antunes-Rodrigues, J.
  • Picanço-Diniz, D. L. W; Universidade Federal do Pará. Centro de Ciências Biológicas. Departamento de Fisiologia. Belém. BR
  • Valença, M. M; Universidade Federal de Pernambuco. Centro de Ciências da Saúde. Departamento de Neurologia e Psiquiatria. Recife. BR
  • Antunes-Rodrigues, J; Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto. Departamento de Fisiologia. Ribeirão Preto. BR
Braz. j. med. biol. res ; 39(11): 1493-1499, Nov. 2006. graf
Article in English | LILACS | ID: lil-437828
Responsible library: BR1.1
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 æM) induced a reduction of PRL secretion into the medium in a U-shaped dose-response curve. The maximal reduction was obtained with 0.1 æM 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 æM = 141.97 ± 15.79 vs control = 244.77 ± 13.79 ng/mg t.w.) of PRL release was blocked by 1 æM cyclopentyltheophylline, a specific A1 receptor antagonist (1 æM = 212.360 ± 26.560 ng/mg t.w.), whereas cyclopentyltheophylline alone (0.01, 0.1, 1 æM) had no effect. R-PIA (0.001, 0.01, 0.1, 1 æM) 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 æM (225.55 ± 71.42 and 201.9 ± 19.08 ng/mg t.w., respectively). Similarly, R-PIA (0.01 æM) 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.
Subject(s)
Full text: Available Index: LILACS (Americas) Main subject: Pituitary Gland, Anterior / Prolactin / Signal Transduction / Adenosine / Receptor, Adenosine A1 Limits: Animals Language: English Journal: Braz. j. med. biol. res Journal subject: Biology / Medicine Year: 2006 Type: Article / Project document Affiliation country: Brazil Institution/Affiliation country: Universidade Federal de Pernambuco/BR / Universidade Federal do Pará/BR / Universidade de São Paulo/BR

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Full text: Available Index: LILACS (Americas) Main subject: Pituitary Gland, Anterior / Prolactin / Signal Transduction / Adenosine / Receptor, Adenosine A1 Limits: Animals Language: English Journal: Braz. j. med. biol. res Journal subject: Biology / Medicine Year: 2006 Type: Article / Project document Affiliation country: Brazil Institution/Affiliation country: Universidade Federal de Pernambuco/BR / Universidade Federal do Pará/BR / Universidade de São Paulo/BR