Could antidepressant modulate behavior and genic expression of myosin, SERCA2 e phospholamban in rats with aortic regurgitation?

• Grant number: 12/24670-2
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: March 01, 2013
• End date: December 31, 2013
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Juliana Irani Fratucci de Gobbi
• Grantee: Lina Abu Alhuda
• Host Institution: Instituto de Biociências (IBB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil

Abstract

Aortic regurgitation (AR), a a volume overload, is characterized by the diastolic reflux of blood from the regurgitating aorta to the left ventricle. This effects results from malfunctioning aortic cusps. The main cause of AR in developing countries is rheumatic fever, including Brazil. There is a strong association between cardiovascular diseases and depression. Selective serotonin reuptake inhibitors (SSRI) are one of the most prescribed antidepressants in the world. Previous studies of our laboratory showed that the utilization of a SSRI, paroxetine, improved cardiac function in rats with subchronic AR and reduced the daily ingestion of hypertonic sodium (NaCl 0,3M). Cardiovascular diseases can determine behaviour changes like increase of anxiety, and it is yet unknown if AR would determine anxiogenic state or anhedonia, incapacity of obtaining pleasure through physical or sensorial experiences. A possible target for SSRI action could be a change in the expression of enzyme isoforms that collaborate in the contractile function of the heart muscle, like the heavy chain of myosine, the sarcoplasmatic reticulum Ca++/ATPase (SERCA2) and it's regulator protein, phospholamban (PLN). Thus, the aim of this project will be studying rats with subchronic AR that will be treated with a SSRI (paroxetine) for 4 weeks over: a) anxiety behaviour parameters tested through the elevated plus-maze, b) if anhedonia state exists, and c) genic expression of ±-myosine and ²-myosine, SERCA2 and PLN in the heart tissue.