GABA mechanisms of the nucleus of the solitary tract regulates the cardiovascular and sympathetic effects of moxonidine

Autor(es)

Alves, Thales B. ^[1] ; Totola, Leonardo T. ^[1] ; Takakura, Ana C. ^[2] ; Colombari, Eduardo ^[3] ; Moreira, Thiago S. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, Sao Paulo, SP - Brazil

^[2] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, Sao Paulo, SP - Brazil

^[3] Sao Paulo State Univ, Sch Dent, Dept Physiol & Pathol, Araraquara, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL; v. 194, p. 1-7, JAN 2016.
• Citações Web of Science: 2

Resumo

The antihypertensive drugs moxonidine and clonidine are alpha(2)-adrenoceptor and imidazoline (I-1) agonists. Previous results from our laboratory have shown that moxonidine can act in the commissural nucleus of the solitary tract (commNTS). In addition, some studies have shown that GABA or glutamate receptor blockade in the RVLM blunted the hypotension produced by these antihypertensive agents in spontaneously hypertensive rats. Therefore, in the present study we verify whether the cardiovascular and sympathetic effects produced by moxonidine in the commNTS are dependent on GABAergic or glutamatergic mechanisms. Mean arterial pressure (MAP) and splanchnic sympathetic nerve activity (sSNA) were recorded in urethane-anesthetized, and artificially-ventilated male Wistar rats (250-350 g). Injection of the GABAA antagonist bicuculline (25 pmol/50 nL) into the commNTS reduced the hypotension as well as the sympathoinhibition elicited by moxonidine. Prior injection of the glutamate receptor antagonist kynurenic acid (2.5 nmo1/50 nL) into the commNTS was not effective in reducing the hypotension and sympathoinhibition elicited by moxonidine. Therefore, we conclude that the hypotensive and sympathoinhibitory effects elicited by microinjection of moxonidine into the commNTS are dependent on GABA receptors, but not ionotropic glutamate receptors. (C) 2015 Elsevier B.V. All rights reserved. (AU)

• Processo FAPESP: 14/22406-1 - Alterações respiratórias anatomofuncionais observadas em um modelo experimental da Doença de Parkinson
• Beneficiário: Ana Carolina Takakura Moreira
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 09/54888-7 - Mecanismos neurais envolvidos na quimiorrecepção
• Beneficiário: Eduardo Colombari
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 13/10573-8 - Mecanismos neurais da superfície ventral do bulbo envolvidos na quimiorrecepção
• Beneficiário: Thiago dos Santos Moreira
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 11/11934-9 - Avaliação das respostas cardiovasculares e simpáticas promovidas pela injeção de moxonidina no núcleo do trato solitário comissural de ratos.
• Beneficiário: Thales Biffe Alves
• Modalidade de apoio: Bolsas no Brasil - Doutorado