Aims: 

We have shown previously that hypertension-related structural and gap junction connexin-43 (GJC ( 43) remodelling is involved in the development of ventricular fibrillation (VF). Clinical and experimental studies suggest antiarrhythmic effects of omega-3 fatty acids (PUFA), however, mechanisms are not fully elucidated. Aim of the study was to examine whether PUFA affect susceptibility of aged spontaneously hypertensive rats (SHR) to VF and expression of GJC ( 43, which ensures cell-to-cell synchronisation.

Methods: 

Male and female 14 month-old PUFA fed (20 mg/day/2 months) SHR and age-matched controls were used. Electrically inducible VF was performed on isolated heart preparation. Myocardial GJC ( 43 was detected using immuno-fluorescence and western blotting (WB) and intercellular synchronisation using ultrastructure examination.

Results: 

PUFA resulted in significant blood pressure reduction in both male and female SHR. All untreated SHR hearts were prone to develop sustained VF. In contrast, VF was suppressed by 57% and 67% in PUFA – treated male and female SHR despite myocardial remodelling, i.e. fibrosis and hypertrophy were not eliminated. Immuno-labelling of GJC ( 43 showed that neither hypertension-related remodelling of GJC ( 43 nor its levels was affected by PUFA. However, WB revealed elevated GJC ( 43 phospho-isoforms. Moreover, cardiomyocyte ultrastructure alterations and impairment of cell-to-cell synchronisation was attenuated in PUFA-treated SHR hearts.

Conclusion: 

PUFA exert clear anti-fibrillating effects in aged male and female SHR, whereby modulation of GJC ( 43 channel function may be one of the mechanisms involved in cardioprotection.

Supported by APVV 51 – 059505.