Key result
Testosterone rapidly shortened action potential duration in isolated guinea pig ventricular myocytes by enhancing IKs and suppressing I(Ca,L) via a nontranscriptional, NO-dependent mechanism.
Population
isolated guinea pig ventricular myocytes
Design
Preclinical
Authors
Loading...
May explain sex differences in QTc; leaves open translation to human arrhythmia risk.
Testosterone shortens action potential duration in ventricular myocytes via nontranscriptional regulation of IKs and I(Ca,L), providing a mechanistic explanation for sex differences in QTc intervals.
Bai et al. (2005) studied this question. Testosterone was evaluated on Action potential duration (APD) and membrane currents. Testosterone rapidly shortened action potential duration in isolated guinea pig ventricular myocytes by enhancing IKs and suppressing I(Ca,L) via a nontranscriptional, NO-dependent mechanism.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: