a release of ACh ( Acetylcholine ) at the synaptic cleft ( 1causesa depolarization ( Action Potential
Either persistent inward current ( for example , through sodium channels ) or reduced outward current ( through potassium channelscan causeprolongation of the action potential
Exposure of isolated myocytes to HNE and acroleincausesprolongation of the action potential
Block of hERG channelcausesprolongation of action potential
from decreased inactivation of the inward Na+ or Ca2 + currents , increased activation of the Ca2 + current , or inhibition of one or more of the outward K+ currentscan resultfrom decreased inactivation of the inward Na+ or Ca2 + currents , increased activation of the Ca2 + current , or inhibition of one or more of the outward K+ currents
activation of calcium currentcausesactivation of calcium current
to as much as 50 % of the [ Na+]i overload associated with the increase in late INa caused by ATX - IIcontributesto as much as 50 % of the [ Na+]i overload associated with the increase in late INa caused by ATX - II
in increased magnitude of Ca2 + influx via l - type Ca2 + channelscan resultin increased magnitude of Ca2 + influx via l - type Ca2 + channels
release of Ca^+ from internal stores which activates a different class of K+ channeltriggersrelease of Ca^+ from internal stores which activates a different class of K+ channel
the occurrence of " early afterdepolarizations " , inducing arrhythmiascan causethe occurrence of " early afterdepolarizations " , inducing arrhythmias
Ventricular arrhythmia(passive) may be caused byVentricular arrhythmia
in the lower values of R and fo in MR - PM compared with MR - FWresultsin the lower values of R and fo in MR - PM compared with MR - FW
in slowly developing increases in the magnitude of Ca2 + transientsalso resultedin slowly developing increases in the magnitude of Ca2 + transients