ELEVATION IN BLOOD PRESSURE INDUCED BY HYPEROSMOTIC STIMULUS INVOLVES PURINERGIC SIGNALING BETWEEN OVLT AND PVN OF RATS

The paraventricular nucleus of the hypothalamus (PVN) plays a critical role in neural control of blood pressure (BP) during hyperosmotic challenges, as it receives a major source of excitatory inputs from sensory circumventricular organs, comprising the organ vasculosum of the lamina terminalis (OVLT). Among the well-described excitatory neurotransmitters that are released in PVN during hyperosmostic challenges, including glutamate and angiotensin, our laboratory has identified a new potential one: the adenosine triphosphate (ATP). Previously, we have shown that purinergic signaling is involved in the control of hyperosmotic-induced sympathoexcitation at the level of the PVN, via activation of P2 receptors. In this context, a question still to be clarified was about the source of ATP release in the neuronal microenvironment of the PVN, but recently we have shown that hyperosmotic stimulus stimulates the release of ATP in the PVN, at least in part, from glial cells. Here we hypothesizes that an additional source of ATP acting as excitatory neurotransmitter on PVN neurons during hyperosmotic challenge originates from the OVLT, as a central sodium-induced pressor response.