| Grant number: | 13/50384-0 |
| Support Opportunities: | Regular Research Grants |
| Start date: | October 01, 2013 |
| End date: | September 30, 2014 |
| Field of knowledge: | Biological Sciences - Physiology - Physiology of Organs and Systems |
| Agreement: | University of Southern California |
| Principal Investigator: | Adriana Castello Costa Girardi |
| Grantee: | Adriana Castello Costa Girardi |
| Principal researcher abroad: | Alicia Ann Mcdonoug |
| Institution abroad: | University of Southern California (USC), United States |
| Host Institution: | Instituto do Coração Professor Euryclides de Jesus Zerbini (INCOR). Hospital das Clínicas da Faculdade de Medicina da USP (HCFMUSP). Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil |
| Associated research grant: | 12/10146-0 - Molecular mechanisms of regulation of the proximal tubular function in hypertension, AP.R |
Abstract
A large body of clinical and experimental evidence documents the importance of the kidney in defining the blood pressure (BP) set point and pathogenesis of hypertension. Body fluid volumes and Na+ balance are maintained by the renal regulation of a series of apical Na+ transporters located along the nephron. Changes in the number and/or intrinsic activity of these transporters affect Na+ reabsorption, body fluid volume and BP. Studies from the Girardi lab provide intriguing evidence that therapies aimed at normalizing blood glucose by mimicking the actions of the incretin hormone glucagon like peptide-1 (GLP-1) also have beneficial effects by regulating renal Na+ transport and BP. Furthermore, studies from the McDonough lab provide evidence that BP can be lowered by either inhibiting Na+ transporters in the proximal nephron (pressure-natriuresis response) or preventing activation of distal nephron transporters. In this context, this collaborative project aims to combine the expertise of two well established labs to determine where and how GLP-1 alters apical Na+ transporters' abundance and covalent modification along the nephron in order to lower BP. Accomplishing this aim will elucidate the precise mechanism of the renal and cardiovascular benefits of incretin-based therapies currently administered to patients with diabetes, obesity or metabolic syndrome, all at risk for cardiovascular diseases. (AU)
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