TY  - JOUR
AU  - Dronjak, Slađana
AU  - Stefanović, Bojana
AU  - Jovanović, Predrag
AU  - Spasojević, Nataša
AU  - Janković, Milica
AU  - Jeremić, Ivica
AU  - Hoffmann, Markus
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1929
AB  - Baseline sympathetic activity was found to be elevated in rheumatoid arthritis (RA) patients and it is related to increased cardiovascular risk in these patients. Although many studies have highlighted the association between RA and increased cardiac sympathetic activity, the underlying mechanistic links remain unclear. The aim of the present study was to understand how diseases-triggered changes in gene expression may result in maladaptive physiological changes. Our results suggest that the equilibrium between noradrenaline synthesis, release and reuptake was disrupted in the ventricles of arthritic rats. In the acute phase of the arthritic process, decreased gene expression of MAO-A might lead to accumulation of noradrenaline in myocardial interstitial space, whereas increased gene expression of NET protected cardiomyocytes from the deleterious effects of enhanced noradrenaline. During the chronic phase, reduced expression of beta(1)-adrenoceptor and decreased efficiency of noradrenaline reuptake contribute to progressive damage of the myocardium and limits heart efficiency.
T2  - Autonomic Neuroscience: Basic and Clinical
T1  - Altered cardiac gene expression of noradrenaline enzymes, transporter and beta-adrenoceptors in rat model of rheumatoid arthritis
VL  - 208
SP  - 165
EP  - 169
DO  - 10.1016/j.autneu.2017.10.003
ER  - 

@article{
author = "Dronjak, Slađana and Stefanović, Bojana and Jovanović, Predrag and Spasojević, Nataša and Janković, Milica and Jeremić, Ivica and Hoffmann, Markus",
year = "2017",
abstract = "Baseline sympathetic activity was found to be elevated in rheumatoid arthritis (RA) patients and it is related to increased cardiovascular risk in these patients. Although many studies have highlighted the association between RA and increased cardiac sympathetic activity, the underlying mechanistic links remain unclear. The aim of the present study was to understand how diseases-triggered changes in gene expression may result in maladaptive physiological changes. Our results suggest that the equilibrium between noradrenaline synthesis, release and reuptake was disrupted in the ventricles of arthritic rats. In the acute phase of the arthritic process, decreased gene expression of MAO-A might lead to accumulation of noradrenaline in myocardial interstitial space, whereas increased gene expression of NET protected cardiomyocytes from the deleterious effects of enhanced noradrenaline. During the chronic phase, reduced expression of beta(1)-adrenoceptor and decreased efficiency of noradrenaline reuptake contribute to progressive damage of the myocardium and limits heart efficiency.",
journal = "Autonomic Neuroscience: Basic and Clinical",
title = "Altered cardiac gene expression of noradrenaline enzymes, transporter and beta-adrenoceptors in rat model of rheumatoid arthritis",
volume = "208",
pages = "165-169",
doi = "10.1016/j.autneu.2017.10.003"
}

Dronjak, S., Stefanović, B., Jovanović, P., Spasojević, N., Janković, M., Jeremić, I.,& Hoffmann, M.. (2017). Altered cardiac gene expression of noradrenaline enzymes, transporter and beta-adrenoceptors in rat model of rheumatoid arthritis. in Autonomic Neuroscience: Basic and Clinical, 208, 165-169.
https://doi.org/10.1016/j.autneu.2017.10.003

Dronjak S, Stefanović B, Jovanović P, Spasojević N, Janković M, Jeremić I, Hoffmann M. Altered cardiac gene expression of noradrenaline enzymes, transporter and beta-adrenoceptors in rat model of rheumatoid arthritis. in Autonomic Neuroscience: Basic and Clinical. 2017;208:165-169.
doi:10.1016/j.autneu.2017.10.003 .

Dronjak, Slađana, Stefanović, Bojana, Jovanović, Predrag, Spasojević, Nataša, Janković, Milica, Jeremić, Ivica, Hoffmann, Markus, "Altered cardiac gene expression of noradrenaline enzymes, transporter and beta-adrenoceptors in rat model of rheumatoid arthritis" in Autonomic Neuroscience: Basic and Clinical, 208 (2017):165-169,
https://doi.org/10.1016/j.autneu.2017.10.003 . .