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- W2117685890 abstract "To the Editor: Geelen and coworkers1 reported 6% to 15% increases in action potential duration in guinea pig hearts exposed to supratherapeutic concentrations (30 μmol/L) of sildenafil. They observed that high concentrations (IC50, 100 μmol/L) inhibited the rapid component of the delayed rectifier K+ current in Chinese hamster ovary and HEK293 cells transfected with human ether-a-go-go-related gene (HERG). Their interpretation that this could lead to adverse cardiovascular effects in humans is unfounded.Sildenafil inhibits the human PDE5 enzyme in vitro by 50% at a concentration of 3.5 nmol/L,2 which is nearly 30 000 times below the level required to block HERG by 50%. Sildenafil is 96% protein-bound, with a peak free plasma concentration after the maximum recommended therapeutic dose (100 mg) of 40 nmol/L,3 which is 2500 times lower than the concentration required to inhibit HERG by 50%.Because sildenafil is metabolized primarily via CYP3A4, the authors imply that during coadministration with CYP3A4 inhibitors (eg, erythromycin), sildenafil plasma levels could rise by 20-fold. However, sildenafil has a high oral bioavailability (≈40%), which limits the extent that coadministered drugs can raise …" @default.
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- W2117685890 date "2001-06-12" @default.
- W2117685890 modified "2023-09-23" @default.
- W2117685890 title "Sildenafil (Viagra) Prolongs Cardiac Repolarization by Blocking the Rapid Component of the Delayed Rectifier Potassium Current" @default.
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- W2117685890 doi "https://doi.org/10.1161/01.cir.103.23.e119" @default.
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