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|Title:||Baroreflex deficiency induces additional impairment of vagal tone, diastolic function and calcium handling proteins after myocardial infarction|
|Authors:||Mostarda, Cristiano [UNIFESP]|
Medeiros, Alessandra [UNIFESP]
Moreira, Edson D.
Moraes-Silva, Ivana Cinthya [UNIFESP]
Brum, Patricia C.
De Angelis, Katia
Irigoyen, Maria Claudia [UNIFESP]
Fed Univ Maranhao UFMA
Sao Judas Tadeu Univ USJT
Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Nove de Julho Univ UNINOVE
calcium handling proteins
|Publisher:||E-century Publishing Corp|
|Citation:||American Journal Of Translational Research. Madison: E-century Publishing Corp, v. 6, n. 3, p. 320-328, 2014.|
|Abstract:||Baroreflex dysfunction has been considered an important mortality predictor after myocardial infarction (MI). However, the impact of baroreflex deficiency prior to MI on tonic autonomic control and cardiac function, and on the profile of proteins associated with intracellular calcium handling has not yet been studied. The aim of the present study was to analyze how the impairment of baroreflex induced by sinoaortic denervation (SAD) prior to MI in rats affects the tonic autonomic control, ventricular function and cardiomyocyte calcium handling proteins. After 15 days of following or SAD surgery, rats underwent MI. Echocardiographic, hemodynamic, autonomic and molecular evaluations were performed 90 days after MI. Baroreflex impairment led to additional damage on: left ventricular remodeling, diastolic function, vagal tonus and intrinsic heart rate after MI. The loss of vagal component of the arterial baroreflex and vagal tonus were correlated with changes in the cardiac proteins involved in intracellular calcium homeostasis. Furthermore, additional increase in sodium calcium exchanger expression levels was associated with impaired diastolic function in experimental animals. Our findings strongly suggest that previous arterial baroreflex deficiency may induce additional impairment of vagal tonus, which was associated with calcium handling proteins abnormalities, probably triggering ventricular diastolic dysfunction after MI in rats.|
|Appears in Collections:||Artigo|
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