AMPA and angiotensin type 1 receptors are necessary for hemorrhage-induced vasopressin secretion

Abstract

Hypovolemia induced by hemorrhage is a common clinical complication, which stimulates vasopressin (AVP) secretion by the neurohypophysis in order to retain body water and maintain blood pressure. To evaluate the role of brain L-glutamate and angiotensin II on AVP secretion induced by hypovolemia we induced hemorrhage (B25% of blood volume) after intracerebroventricular (icv) administration of AP5, NBQX, or losartan, which are NMDA, AMPA, and AT1 receptor antagonists, respectively. Hemorrhage significantly increased plasma AVP levels in all groups. The icv injection of AP5 did not change AVP secretion in response to hemorrhage. Conversely, icv administration of both NBQX and losartan significantly decreased plasma AVP levels after hemorrhage. Therefore, the blockade of AMPA and AT1 receptors impaired AVP secretion in response to hemorrhage, suggesting that L-glutamate and angiotensin II acted in these receptors to increase AVP secretion in response to hemorrhage-induced hypovolemia.

Osmoregulation and the Hypothalamic Supraoptic Nucleus: From Genes to Functions

“…By using intra-SON microinjection, Busnardo et al (2012) demonstrated that AVP and OXT secretion is mediated by AMPA receptors. In this context, it has recently been shown in in vivo experiments that hyperosmolality and hemorrhage affect AVP secretion through activation of NMDA and AMPA receptors ( Vilhena-Franco et al, 2018 ; Busnardo et al, 2021 ; Dos-Santos et al, 2022 ). Those findings indicate that the MNCs are subject to the influence of both l -glutamate and GABA activated channels and that their close interaction with astrocytes is essential to integrate the osmoreception process in the SON.…”