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Collaborative effort to determine the molecular bases of the blood pressure lowering effects of the incretin hormone GLP-1

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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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Publicações científicas
(Referências obtidas automaticamente do Web of Science e do SciELO, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores)
CARNEIRO DE MORAIS, CARLA P.; POLIDORO, JULIANO Z.; RALPH, DONNA L.; PESSOA, THAISSA D.; OLIVEIRA-SOUZA, MARIA; BARAUNA, VALERIO G.; REBOUCAS, NANCY A.; MALNIC, GERHARD; MCDONOUGH, ALICIA A.; GIRARDI, ADRIANA C. C. Proximal tubule NHE3 activity is inhibited by beta-arrestin-biased angiotensin II type 1 receptor signaling. AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, v. 309, n. 8, p. C541-C550, OCT 15 2015. Citações Web of Science: 4.

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