thiourea and Tachycardia--Supraventricular

thiourea has been researched along with Tachycardia--Supraventricular* in 1 studies

Other Studies

1 other study(ies) available for thiourea and Tachycardia--Supraventricular

Article	Year
An increase of late sodium current induces delayed afterdepolarizations and sustained triggered activity in atrial myocytes. American journal of physiology. Heart and circulatory physiology, 2008, Volume: 294, Issue:5 This study determined the role of a slowly inactivating component of sodium current (I(Na)), late I(Na), to induce delayed afterdepolarizations (DADs) and triggered activity. We hypothesized that an increase of late I(Na) may induce not only early afterdepolarizations (EADs), but also intracellular calcium overload and DADs. Guinea pig atrial myocytes were studied using the whole cell patch-clamp technique. Anemone toxin II (ATX-II) (5-10 nmol/l) was used to enhance late I(Na). Ranolazine (10 micromol/l) and TTX (2 micromol/l) were applied to block ATX-II-induced late I(Na). ATX-II prolonged action potential duration and induced EADs. In the continuous presence of ATX-II, following the appearance of EADs, both DADs and sustained triggered activity occurred. Triggered activity was abolished and DADs were reduced by either ranolazine or TTX. Consistent with induction of DADs, ATX-II induced the transient inward current (I(TI)). The amplitude of I(TI) was significantly reduced by ranolazine. ATX-II induced only EADs, but no DADs, in the presence of the sodium-calcium exchange inhibitor KB-R7943 or the sarcoplasmic reticulum calcium release channel inhibitor ryanodine, or when the calcium chelator EGTA or BAPTA was included in the pipette solution. In conclusion, an increase of late I(Na), in addition to inducing EADs, can cause cellular calcium overload and induce DADs and sustained triggered activity in atrial myocytes. The data reveal that an increase of late I(Na) is a novel mechanism for initiation of atrial arrhythmic activity. Topics: Acetanilides; Action Potentials; Animals; Anti-Arrhythmia Agents; Calcium; Cardiotonic Agents; Chelating Agents; Cnidarian Venoms; Egtazic Acid; Guinea Pigs; Heart Atria; Heart Conduction System; Myocytes, Cardiac; Patch-Clamp Techniques; Piperazines; Ranolazine; Ryanodine; Ryanodine Receptor Calcium Release Channel; Sodium; Sodium Channel Blockers; Sodium Channels; Sodium-Calcium Exchanger; Tachycardia, Supraventricular; Tetrodotoxin; Thiourea; Time Factors; Up-Regulation	2008

Article

Year

An increase of late sodium current induces delayed afterdepolarizations and sustained triggered activity in atrial myocytes.

American journal of physiology. Heart and circulatory physiology, 2008, Volume: 294, Issue:5

This study determined the role of a slowly inactivating component of sodium current (I(Na)), late I(Na), to induce delayed afterdepolarizations (DADs) and triggered activity. We hypothesized that an increase of late I(Na) may induce not only early afterdepolarizations (EADs), but also intracellular calcium overload and DADs. Guinea pig atrial myocytes were studied using the whole cell patch-clamp technique. Anemone toxin II (ATX-II) (5-10 nmol/l) was used to enhance late I(Na). Ranolazine (10 micromol/l) and TTX (2 micromol/l) were applied to block ATX-II-induced late I(Na). ATX-II prolonged action potential duration and induced EADs. In the continuous presence of ATX-II, following the appearance of EADs, both DADs and sustained triggered activity occurred. Triggered activity was abolished and DADs were reduced by either ranolazine or TTX. Consistent with induction of DADs, ATX-II induced the transient inward current (I(TI)). The amplitude of I(TI) was significantly reduced by ranolazine. ATX-II induced only EADs, but no DADs, in the presence of the sodium-calcium exchange inhibitor KB-R7943 or the sarcoplasmic reticulum calcium release channel inhibitor ryanodine, or when the calcium chelator EGTA or BAPTA was included in the pipette solution. In conclusion, an increase of late I(Na), in addition to inducing EADs, can cause cellular calcium overload and induce DADs and sustained triggered activity in atrial myocytes. The data reveal that an increase of late I(Na) is a novel mechanism for initiation of atrial arrhythmic activity.

Topics: Acetanilides; Action Potentials; Animals; Anti-Arrhythmia Agents; Calcium; Cardiotonic Agents; Chelating Agents; Cnidarian Venoms; Egtazic Acid; Guinea Pigs; Heart Atria; Heart Conduction System; Myocytes, Cardiac; Patch-Clamp Techniques; Piperazines; Ranolazine; Ryanodine; Ryanodine Receptor Calcium Release Channel; Sodium; Sodium Channel Blockers; Sodium Channels; Sodium-Calcium Exchanger; Tachycardia, Supraventricular; Tetrodotoxin; Thiourea; Time Factors; Up-Regulation

2008