CARDIOPROTECTIVE EFFECTS OF FINERENONE ASSOCIATED WITH THE SUPPRESSION OF MYOCARDIAL SODIUM ACCUMULATION IN ALDOSTERONE/SALT-LOADED RATS

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https://storage.unitedwebnetwork.com/files/1099/5f05b426d820fc5d1afd28dcfe31c946.pdf

Abstract Title *

CARDIOPROTECTIVE EFFECTS OF FINERENONE ASSOCIATED WITH THE SUPPRESSION OF MYOCARDIAL SODIUM ACCUMULATION IN ALDOSTERONE/SALT-LOADED RATS

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Co-author 1

Kento Kitada kitada.kento@kagawa-u.ac.jp Faculty of Medicine, Kagawa University Department of Pharmacology Kagawa Japan -

Co-author 2

Asadur Rahman rahman.md.asadur@kagawa-u.ac.jp Faculty of Medicine, Kagawa University Department of Pharmacology Kagawa Japan -

Co-author 3

Akira Nishiyama nishiyama.akira@kagawa-u.ac.jp Faculty of Medicine, Kagawa University Department of Pharmacology Kagawa Japan *

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Introduction

Finerenone, a nonsteroidal mineralocorticoid receptor antagonist, has demonstrated considerable cardiovascular protective benefits in clinical trials; however, its precise mechanism of action remains to be fully elucidated.

Methods

Here, we examined the impact of finerenone on myocardial injury and sodium accumulation in uninephrectomized (UNx) Sprague-Dawley (SD) rats subjected to chronic aldosterone infusion (0.75 µg/hr) and salt-loading (1% NaCl) through drinking water over a period of 4 weeks.

Results

Echocardiographic assessments and gene expression analyses revealed adverse cardiac remodeling and ventricular dysfunction with preserved ejection fraction. Notably, finerenone treatment completely prevented the development of cardiac dysfunction in these animals. Additionally, sodium content in left ventricular tissues was markedly elevated in aldosterone/salt-loaded UNx SD rats, which was inhibited by finerenone treatment. Furthermore, significant increase in macrophage recruitment was observed in cardiac tissues of aldosterone-salt loaded rats with markedly elevated M1 macrophage populations. However, finerenone treatment effectively prevented migration as well as polarization of macrophage in cardiac tissue. In an in vitro assay using RAW264.7 cells, finerenone dramatically reduced the aldosterone/salt-induced elevation of M1 markers, while M2 markers exhibited a tendency to increase, potentially linked to NFAT5 and IL-10 mediated pathways.

Conclusion

These findings suggest that finerenone has the potential to mitigate cardiac dysfunction in aldosterone/salt-loaded rats by suppressing sodium accumulation in left ventricular tissues and attenuate subsequent macrophage-mediated inflammation, thereby preventing adverse cardiac remodeling and dysfunction.

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