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Influence of the angiotensin receptor AT1 knockdown over the alpha-2 adrenoceptor in the nucleus of the solitary tract

Grant number: 13/11542-9
Support Opportunities:Scholarships abroad - Research Internship - Doctorate
Start date: November 01, 2013
End date: April 30, 2014
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Debora Rejane Fior Chadi
Grantee:Sergio Marinho da Silva
Supervisor: Mohan K. Raizada
Host Institution: Instituto de Biociências (IB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Institution abroad: University of Florida, Gainesville (UF), United States  
Associated to the scholarship:09/18564-2 - Modulation of glutamatergic and cathecolaminergic systems by glutamate in the nucleus of the solitary tract. Analysis in the adult and in cell culture of the brainstem, BP.DR

Abstract

The alpha-2 adrenoceptor (alpha2r) and the angiotensin 2 receptor AT1 (AT1r) in the nucleus of the solitary tract (NTS) have pivotal importance in the regulation of the baroreflex. Both receptors induce changes in the arterial pressure and baroreflex sensitivity upon stimulation.It is known that AT1r activation reduces the alpha2r affinity in the NTS, which indicates that not only these receptors interact among each other, but that this interaction could modulate the central regulation of the arterial pressure.However, little is known about how the AT1r modulates the alpha2r, and how this modulation could interfere with the baroreflex. Given that AT1r are also very important in the central regulation of the arterial pressure, and taking into consideration that circulatory angiotensin II could regulate, though indirectly, the NTS through the circumventricular organs, we would like to study the influence of the AT1r over the alpha2r in the nucleus of the solitary tract of 3-month old rats. In order to observe how the presence or absence of the AT1 receptor could be relevant to the alpha2r, we propose to administer angiotensin II into the NTS, as well as knockdown the AT1r, and analyze its influence over the alpha2r protein levels through Western Blotting assay. We believe that this analysis could help us understand how the crosstalk between AT1r and alpha2r can modulate the regulation of the arterial pressure. (AU)

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