Papel dos receptores andrenérgicos da preóptica medial (APM) no controle da salivação induzida pela ativação colinérgica em ratos.

• Ano de defesa: 2004
• Autor(a) principal: Almeida, Roberto Lopes de
• Orientador(a): Renzi, Antonio
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de São Carlos
• Programa de Pós-Graduação: Programa Interinstitucional de Pós-Graduação em Ciências Fisiológicas - PIPGCF
• País: BR
• Palavras-chave em Português: Glândulas salivares; Pilocarpina; Noradrenalina; Salivação; APM
• Área do conhecimento CNPq: CIENCIAS BIOLOGICAS::FISIOLOGIA
• Link de acesso: https://repositorio.ufscar.br/handle/ufscar/1367

The present work had as objective to investigate the participation of the mechanisms adrenergics of the medial preoptic area (APM) in the salivary secretion induced for the peripheral colinergic stimulation (pilocarpine injection). Holtzman rats had been used (280-320 g). A part of the animals suffered electrolytic lesion in the APM through the ticket from electric chain (1mA x 3x10s), to serve as control, and another part of the animals was submitted to the same procedures of cerebral surgery, except that it was not displayed to the electric chain ticket (SHAM). Animals that suffered the surgery from implant of cannulas guides in the APM for the injection of adrenergics agonists and antagonists were also used. The saliva was collected using previously weighted and inserted balls of cotton in the mouth of the animal that was under anesthesia with quetamina (1mg/mL/kg). Salivation was induced for intraperitoneal injection (IP) of pilocarpine (1mg/mL/kg). The APM lesion in such a way reduced peripheral the pilocarpine-induced salivation group that suffered APM lesion 24 hours before the experiment (APM lesion 340,7 ± 41,1 mg/7min, versus SHAM 428,4 ± 31,6 mg/7min) as much as in the group that suffered APM lesion 5 days before the experiment (APM lesion 310,2 ± 35,4 mg/7min, versus SHAM 494,9 ± 35,5 mg/7min). Reduction in the peripheral pilocarpine-induced salivation was not verified in those animals that had suffered APM lesion 15 days before the experiment (APM lesion 461,6 ± 81,4 mg/7min, versus SHAM 575,7 ± 34,9 mg/7min). The injection of noradrenaline (80 nmol/0,5µL) in the APM did not reduce the peripheral pilocarpine-induced salivation (NOR + Pilo 356,0 ± 36,0 mg/7min versus Saline + Pilo 475,0 ± 73,0 mg/7min). This same drug in the dose of 160 nmol/0,5 µL reduced the peripheral pilocarpine-induced salivation (NOR + Pilo 251,0 ± 50,0 mg/7min versus Saline + Pilo 468,0 ± 59,0 mg/7min). The inhibitory effect of the injection in the APM of noradrenaline (160 nmol/0,5µL) in the peripheral pilocarpine-induced salivation was not reduced by the previous injection of the antagonist of adrenoceptors α2, RX-821002 in the dose of 80 nmol/0,5µL (RX + NOR + Pilo 244,1 ± 29,2 mg/7 min, versus Saline + NOR + Pilo 202,3 ± 34,8 mg/7 min). On the other hand, this same drug injected in the dose of 160 nmol/0,5µL, partially reverted the inhibitory effect of the injection in the APM of noradrenalina (160 nmol/0,5µL) in the peripheral pilocarpine-induced salivation (RX + NOR + Pilo 329,9 ± 77,8 mg/7min, versus Saline + NOR + Pilo 148,2 ± 30,3 mg/7min). The RX- 821002 injected in the APM in the dose of 320 nmol/0,5µL, failed in showing the reversion of the inhibitory effect of the injection in the APM of noradrenaline (160nmol/0,5µL) in the peripheral pilocarpine-induced salivation (RX + NOR + 261,3 ± 18,9 mg/7min, versus Saline + NOR + Pilo 320,4 ± 30,2 mg/7min). The antagonist of adrenergics receptors α1, Prazosin, did not reveal efficient, therefore the inhibitory effect of the injection in the APM of noradrenaline (160 nmol/0,5µL) in the peripheral pilocarpine-induced salivation was not reduced by the previous injection of the adrenergic antagonist α1, Prazosin, in the dose of 160 nmol/0,5µL (Prazosin + NOR + Pilo 223,6 ± 35,8 mg/7min, versus Saline + NOR + Pilo 256,0 ± 58,5 mg/7min). The results show that the noradrenaline injected in the APM reduces the peripheral pilocarpine-induced salivation and this effect is reduced by the previous blockade of the receiving adrenergics α2 of the same area, suggesting to the existence of an adrenergic α2 inhibitory mechanism of the salivation in the APM.