Evaluation of the adenosine triphosphate content in the hypothalamus of salt-induced hypertensive animal model

• Grant number: 19/10312-6
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Effective date (Start): August 01, 2019
• Effective date (End): September 30, 2020
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Vagner Roberto Antunes
• Grantee: Zaira Maria de Sousa Pinheiro
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

One of the key fuction of the cardiovascular system is to control the blood flow to different territories in the body for the maintenance of organic homeostasis. The arterial pressure(AP) is the driving force of the blood flow and its levels depend directly on the heart contractility and rate, and vascular peripheral resistance, both regulated by neural, hormonal and renal mechanisms. It is well established that increasing in osmolality, due to a high salt intake, leads to rise in the blood pressure associated to an increase in the sympathetic nerve activity (SNA), named as neurogenic hypertension. The changes in osmolality are detected by the osmoreceptors located in central nervous system (CNS), in structures called as circumventricular organs (CVOs) that maintains direct connections with the hypothalamic paraventricular nucleus (PVN). The PVN is composed by a subpopulations of magnocelularand parvocellular neurons with projections in the rostral ventrolateral medulla (RVLM) and/orin the intermediolateral column (IML), a neuronal network with direct involvement in control of the SNA and blood pressure. Recent studies from our laboratory have shown that adenosine triphosphate (ATP) participates in the signaling of neuronal groups in the PVN.It was also showed that ATP elevates the frequency of action potentials in PV presympathetic neurons. Thus, the sympatho-excitatory response elicited by the increase of plasmatic osmolality can be related to the activation of purine-glutamatergic mechanisms in PVN parasympathetic neurons. One of the questions that still remains is about the source ofATP as a neurotransmitter, and whether the availability of this purine at the hypothalamic level would be increased during hyperosmotic stimulus with salt-loading, and this is the answer we are proposing to investigate in this scientific project.