Extracellular acidification reveals the antiarrhythmic properties of amiodarone related to late sodium current-induced atrial arrhythmia.

Background: Amiodarone (AMIO) is an antiarrhythmic drug with the pKa in the physiological range. Here, we explored how mild extracellular pH (pHe) changes shape the interaction of AMIO with atrial tissue and impact its pharmacological properties in the classical model of sea anemone sodium channel neurotoxin type 2 (ATX) induced late sodium current (I) and arrhythmias.

Method: Isolated atrial cardiomyocytes from male Wistar rats and human embryonic kidney cells expressing SCN5A Na channels were used for patch-clamp experiments.

The fungicide tebuconazole modulates the sodium current of human Na1.5 channels expressed in HEK293 cells.

The fungicide Tebuconazole is a widely used pesticide in agriculture and may cause cardiotoxicity. In our present investigation the effect of Tebuconazole on the sodium current (I) of human cardiac sodium channels (Na1.5) was studied using a heterologous expression system and whole-cell patch-clamp techniques.

Evaluation of right atrium structure and function in a rat model of monocrotaline-induced pulmonary hypertension: Exploring the possible antiarrhythmic properties of amiodarone.

Atrial arrhythmias (AA) are common in pulmonary hypertension (PH) and are closely associated with poor clinical outcomes. One of the most studied models to investigate PH is the rat model of monocrotaline (MCT) induced PH (MCT-PH). To date, little is known about right atrium (RA) function in the MCT-PH model and the propensity of RA to develop arrhythmias.