Interaction of angiotensin II and endothelins 1 or 3 on the control of rennin secretion and sodium transporters in renal cells.

• Grant number: 11/19300-9
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: December 01, 2011
• End date: November 30, 2012
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Maria Oliveira de Souza
• Grantee: Tamires da Silva Braga
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

In physiological conditions, the angiotensin II (Ang II) regulates the blood pressure and extracellular volume (Weir et al, 1999). These effects are related with maintenance of vascular resistance, renal hemodynamics and renal sodium reabsorption (Kurtz et al., 1999; Spat and Hunydy, 2004). High doses of Ang II elicit the stimulation of AT1 receptor and Endothelin -1 (ET-1) synthesis/secretion. ET-1 via ATb receptor can reduces the rennin secretion in justaglomerular cells and it also stimulates the natriuresis (Takagi et al., 1988; Kohan et al, 2011). On the other hand, endothelin 3 (ET-3) can interacts only with ATb receptors, protein abundantly express in renal tissue, which the effect of ET-3 was not related. Considering the relevance of the biologycal interaction between both Ang II and ETs systems on hemodynamics and renal function, the aim of this study is invetigate the effect of Ang II on the ET-1 and ET-3 secretion and sodium transporters expression. Following, the effect of ET-1 and ET-3 on rennin secretion and sodium transporters expression will also be investigated. Our studies will be achieved in LLcPK1 and MDCK cells. In chronic treatment with Ang II we can evaluate the effect of Ang II on the ET-1 and ET-3 synthesis and consequentially, on the control of rennin secretion, as well sodium transporters expression. In chronic treatment with ET-1 and ET-3 we can evaluate the distinct effects of both peptides on the rennin secretion and sodium transporters expression.