Contribution of the pre-Bötzinger complex to baro-activated CVLM neurons

• Grant number: 12/18841-9
• Support Opportunities: Scholarships abroad - Research Internship - Doctorate
• Start date: March 01, 2013
• End date: February 28, 2014
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Eduardo Colombari
• Grantee: Thales Biffe Alves
• Supervisor: Ann M. Schreihofer
• Host Institution: Faculdade de Odontologia (FOAr). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil
• Institution abroad: UNT Health Science Center, United States
• Associated to the scholarship: 11/11934-9 - Evaluation of cardiovascular and sympathetic responses promoted by moxonidine injection in the commissural nucleus of the solitary tract in rats., BP.DR

Abstract

The sympathetic nerve activity (SNA) that promotes constriction of blood vessels and maintains arterial pressure (AP) is tightly regulated by the brain. However, disruptions in the control of SNA likely contribute to some forms of essential hypertension. This project uses state-of-the-art electrophysiological and anatomical approaches to unravel brain stem mechanisms that regulate SNA and AP in rats. Determining central mechanisms underlying the control of SNA is necessary to further our understanding of the basis for and treatment of essential hypertension. Exposure to chronic intermittent hypoxia (CIH) leads to elevated sympathetic nerve activity (SNA) and arterial pressure (AP), which increases the risk of morbidity and mortality. The mechanisms for elevated SNA are unknown, but a rise in central respiratory drive is likely to contribute. This SNA is modulated by central respiratory neurons that contribute to basal SNA and evoked sympathetic responses. However, elucidating roles of central respiratory neurons for hypoxia-evoked changes in SNA requires a better understanding of the coupling between central respiratory and cardiovascular regulatory neurons. Thus, the knowledge of the function of respiratory neurons on the changes in sympathetic activity aimed at a better understanding of possible causes of treatment for hypertension caused by the exposure to low oxygen concentrations. (AU)