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. 2014 May 15;6(3):320-8.
eCollection 2014.

Baroreflex deficiency induces additional impairment of vagal tone, diastolic function and calcium handling proteins after myocardial infarction

Cristiano Mostarda  1 , Bruno Rodrigues  2 , Alessandra Medeiros  3 , Edson D Moreira  4 , Ivana C Moraes-Silva  4 , Patricia C Brum  5 , Katia De Angelis  6 , Maria-Cláudia Irigoyen  4
Affiliations

Baroreflex deficiency induces additional impairment of vagal tone, diastolic function and calcium handling proteins after myocardial infarction

Cristiano Mostarda et al. Am J Transl Res. .

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.

Keywords: Arterial baroreflex; autonomic tone; calcium handling proteins; cardiac function; cardiac remodeling; myocardial infarction.

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Figures

Figure 1
Figure 1
Expression levels of regulatory proteins related to intracellular calcium homeostasis from Control (C), myocardial infarction (MI) and sinoaortic denervation+MI (SAD+MI). Targeted bands were normalized to cardiac GAPDH. A: Representative blot of GAPDH; B: Sarcoplasmic reticulum calcium ATPase pump (SERCA2); C: Phospholamban (PLN); D: PLN phosphorylated at serine 16 (PLNser16 ); E: PLN phosphorylated at threonine 17 (PLNthr17); F: SERCA2/PLN ratio. *p<0.05 vs. C.
Figure 2
Figure 2
Expression levels of intracellular calcium efflux mediators from Control (C), myocardial infarction (MI) and sinoaortic denervation+MI (SAD+MI). Targeted bands were normalized to cardiac GAPDH (blot represented in Figure 1A). A: Sodium calcium exchanger (NCX); B: SERCA2/NCX ratio; C: Phosphatase protein 1 (PP1); D: Phosphatase protein 2 (PP2A). *p<0.05 vs. C; †p<0.05 vs. MI.
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