1. In the present study, we investigated the effects of @entity273 ( @entity274 ) on the @entity973 -sensitive transient outward current (I(TO)) in @entity95 atrial myocytes using the @entity2379 -perforated patch voltage-clamp method. 2. Superfusion of myocytes with @entity274 at 100 micromol/L gradually slowed the time-course of inactivation of I(TO) and increased the peak by 9% (n = 9). The @entity274 -induced slowing of I(TO) inactivation was concentration dependent (over the concentration range 10 micromol/L to 1 mmol/L). These effects were hardly reversed by washout of @entity274 , but were quickly abolished by @entity3902 (2 mmol/L). 3. @entity30825 (100 nmol/L), an inhibitor of protein kinase C, significantly attenuated the @entity274 -induced effects on I(TO). 4. These results suggest that @entity95 atrial I(TO) is susceptible to oxidation by @entity274 at concentrations relevant to those encountered during ischaemia/reperfusion and that protein kinase C modulates the effects of @entity274 .

Effects of XXXX on the transient outward current in @entity95 atrial myocytes.

@entity274 :: ('CHEBI:16240', 'Chemical') :: ['H2O2'] @entity2379 :: ('MESH:D000666', 'Chemical') :: ['amphotericin B'] @entity3902 :: ('MESH:D004229', 'Chemical') :: ['dithiothreitol'] @entity95 :: ('9986', 'Species') :: ['rabbit'] @entity273 :: ('MESH:D006861', 'Chemical') :: ['hydrogen peroxide'] @entity30825 :: ('MESH:C088060', 'Chemical') :: ['Bisindolylmaleimide'] @entity973 :: ('MESH:D015761', 'Chemical') :: ['4-aminopyridine']
@entity273 :: (MESH:D006861,Chemical) :: ['hydrogen peroxide']
