Hormonal Control of Cardiac Action Potential Phase 1 Currents in the Brugada Syndrome

The study investigated the role of androgens in regulating phase 1 of the cardiac action potential in Brugada Syndrome, a hereditary channelopathy with a male-to-female ratio of 9:1. Using a rat heart model, researchers found that dihydrotestosterone increased the expression of Kv4.3 and NCX in HL-1 cells. Testosterone treatment in rats increased NCX mRNA levels and shortened APD90 and TTP, correlating with increased arrhythmogenicity. Conversely, Finasteride reduced the expression of both genes and significantly decreased the frequency of ectopic action potentials induced by Terfenadine and Pinacidil, suggesting a potential therapeutic effect in reducing arrhythmias associated with Brugada Syndrome.