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Communication between the central nervous system and kidneys: cardiovascular, renal and autonomic influences in physiological and physiopathological conditions

Grant number: 19/25295-0
Support type:Research Projects - Thematic Grants
Duration: March 01, 2021 - February 28, 2026
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Ruy Ribeiro de Campos Junior
Grantee:Ruy Ribeiro de Campos Junior
Home Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil
Co-Principal Investigators:Cassia Marta de Toledo Bergamaschi
Assoc. researchers:Erika Emy Nishi ; Ita Pfeferman Heilberg ; Jean Faber Ferreira de Abreu ; Mark Maurer Knuepfer

Abstract

Cardiovascular and renal diseases are among the main causes of morbidity and mortality in Brazil and worldwide. Hypertension is one of the major risk factors for diseases such as myocardial infarction, renal failure and heart failure. It is interesting that these pathophysiological conditions have in common the increase of sympathetic vasomotor activity and curiously, the greater the severity of cardiovascular and renal disease, the greater the sympathetic vasomotor activation. However, the mechanisms triggering the exacerbated increase in sympathetic vasomotor activity in these conditions are not fully known. In the present project, we intend to advance the understanding of how sympathetic vasomotor activity increases in experimental hypertension and in other models that are known to have an increase in sympathetic activity, especially as the reciprocal communication between the kidneys and the central nervous system (CNS) occurs. The kidneys receive intense sympathetic innervation, which has the ability to change renal function in a robust way and reciprocally, the kidneys contain renal afferents that protrude to the CNS in regions that in turn control the cardiovascular and renal systems. Our hypothesis is that alterations in renal receptors (mechanoreceptors and chemoreceptors) under pathophysiological conditions can trigger alterations in the mechanisms of cardiovascular and renal control leading to sympathetic overactivation under pathophysiological conditions, aggravating and worsening the condition. We hope that at the end of this project we can advance in the understanding of how the sympathetic vasomotor activity increases disproportionately in some pathophysiological situations, especially with regard to communication between CNS and kidneys. (AU)