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Effect of interaction between renin-angiotensin-aldosterone system and endothelin 1 and 3 on renal function

Grant number: 11/14022-0
Support type:Scholarships in Brazil - Doctorate
Effective date (Start): March 01, 2012
Effective date (End): September 30, 2015
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal researcher:Maria Oliveira de Souza
Grantee:Fernando Augusto Malavazzi Casare
Home Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

The renin-angiotensin-aldosterone system (SRAA) regulates the blood pressure and extracellular volume. Its activity depends of the enzyme renin, that increases the angiotensin II (Ang II) plasma levels. Ang II has a positive effect on aldosterone secretion. Both Ang II and aldosterone stimulate the renal sodium reabsorption (Kurtz et al., 1999; Spat and Hunydy, 2004). High doses of Ang II elicit hypertension and sodium rabsorption. In this condition, Ang II regulates many intracellular signaling pathways to induce growth and proinflammatory responses in different tissues. Ang II also induces synthesis of reactive oxygen species (ROS) (Timmermans et al, 1993; Rhian et al, 2000; Navar et al., 2000; Castrop et al., 2010). Chronic Ang II infusion induces apoptosis of podocites and change the nephrin mRNA expression with subsequent proteinuria (Ding et al., 2008). In the kidney, ET-1 via ATa receptor can regulate the renal hemodynamics (Karet & Devenport, 1996, Kohan, 2010) and via ATb receptor the ET-1 can modulate the renal sodium and water transport (Kohan & Padilla, 1993; Kuc & Davenport, 2004; Wesson, 2001). At high doses ET-1 as Ang II, modulates intracellular signaling pathways to induce growth and proinflammatory response associated with renal pathologies (Endemann & Schiffrin, 2004; Kohan, 2010). However, the effect of ET-3 by ET-b receptor on renal function has not been investigated. Considering the relevance of the biological interaction between both SRAA and ETs systems on hemodynamics and renal function, the aim of this study is to investigate the effect of interaction between Ang II and ETs on renin and aldosteron secretion, renal hemodynamics and tubular functions, sodium transport expression and renal tissue injury. (AU)

Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
CARDOSO, VANESSA GEROLDE; GONCALVES, GUILHERME LOPES; COSTA-PESSOA, JULIANA MARTINS; THIEME, KARINA; LINS, BRUNA BEZERRA; MALAVAZZI CASARE, FERNANDO AUGUSTO; DE PONTE, MARIANA CHARLEAUX; SARAIVA CAMARA, NIELS OLSEN; OLIVEIRA-SOUZA, MARIA. Angiotensin II-induced podocyte apoptosis is mediated by endoplasmic reticulum stress/PKC-delta/p38 MAPK pathway activation and trough increased Na+/H+ exchanger isoform 1 activity. BMC Nephrology, v. 19, JUL 13 2018. Web of Science Citations: 7.
DE PONTE, MARIANA CHARLEAUX; MALAVAZZI CASARE, FERNANDO AUGUSTO; COSTA-PESSOA, JULIANA MARTINS; CARDOSO, VANESSA GEROLDE; MALNIC, GERHARD; MELLO-AIRES, MARGARIDA; VOLPINI, RILDO APARECIDO; THIEME, KARINA; OLIVEIRA-SOUZA, MARIA. The Role of beta-Adrenergic Overstimulation in the Early Stages of Renal Injury. Kidney & Blood Pressure Research, v. 42, n. 6, p. 1277-1289, 2017. Web of Science Citations: 1.
MALAVAZZI CASARE, FERNANDO AUGUSTO; THIEME, KARINA; COSTA-PESSOA, JULIANA MARTINS; ROSSONI, LUCIANA VENTURINI; COUTO, GISELE KRUGER; FERNANDES, FERNANDA BARRINHA; CASARINI, DULCE ELENA; OLIVEIRA-SOUZA, MARIA. Renovascular remodeling and renal injury after extended angiotensin II infusion. AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, v. 310, n. 11, p. F1295-F1307, JUN 1 2016. Web of Science Citations: 11.
Academic Publications
(References retrieved automatically from State of São Paulo Research Institutions)
CASARE, Fernando Augusto Malavazzi. Effect of interaction of Angiotensin II and AT1 receptor, or endothelin 3 and ETA and ETB receptors on renal function and morphology in rats.. 2015. Doctoral Thesis - Universidade de São Paulo (USP). Instituto de Ciências Biomédicas São Paulo.

Please report errors in scientific publications list by writing to: cdi@fapesp.br.