Role of AMPA and NMDA receptors on vasopressin and oxytocin secretion induced by hypertonic extracellular volume expansion

Autor(es)

Vilhena-Franco, Tatiane ; Valentim-Lima, Evandro ; Reis, Luis C. ; Elias, Lucila L. K. ; Antunes-Rodrigues, Jose ; Mecawi, Andre S.

• Tipo de documento: Artigo Científico
• Fonte: Journal of Neuroendocrinology; v. 30, n. 8, p. 7-pg., 2018-08-01.

Resumo

Vasopressin (AVP) and oxytocin (OT) are essential for the control of extracellular fluid osmolality and volume. The secretion of these hormones is modulated by several mechanisms, including NMDA and AMPA L-glutamate receptors in magnocellular cells of paraventricular (PVN) and supraoptic (SON) hypothalamic nuclei. Thus, to better understand the participation of i-glutamate on the neuroendocrine control of AVP and OT, the present study evaluated the effects of i.c.v. NMDA and AMPA receptor antagonists on plasma AVP and OT levels induced by extracellular volume expansion (EVE). Cannulated rats received i.c.v. NMDA (amino-5-phosphonovalerate; AP5) and AMPA (2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo[f]quinoxaline; NBQX) antagonists in doses of 10 and 30 nmol (5 mu L per rat) and were subjected to either isotonic (0.15 mol L-1 NaCl, 2 mL per 100 g) or hypertonic (0.30 mol L-1 NaCl, 2 mL per 100 g) EVE. Blood samples were collected for plasma AVP and OT determination. Isotonic EVE did not change plasma AVP and OT levels, although hypertonic EVE increased both AVP and OT plasma levels. AP5 reduced plasma AVP, although it did not change the OT level induced by hypertonic EVE. On the other hand, NBQX reduced plasma OT but did not alter the AVP plasma level. Our data show that L-glutamate controls the secretion of neurohypophyseal hormones via the NMDA receptor for AVP release, as well as via the AMPA receptor for OT release, both in response to hypertonic EVE. (AU)

• Processo FAPESP: 13/09799-1 - Regulação da homeostase energética e do balanço hidromineral: das células aos sistemas fisiológicos
• Beneficiário: José Antunes Rodrigues
• Modalidade de apoio: Auxílio à Pesquisa - Temático