I have more than 6 years of experience in teaching and research. In many diseased condition drugs treatment leads to drug-induced cardiac arrhythmia and cardiomyopathy which shows pathological changes in the cardiomyocytes. In cardiomyocytes, Angiotensin II (AngII) triggers cellular signaling by binding to its receptors: angiotensin II type I receptor (AT1R) and angiotensin II type II receptor (AT2R). The physiological effect of Ang II is mainly transduced by its binding with AT1R. Ang II controls electrolyte balance and blood pressure by stimulating the heart to release aldosterone. Ang II is also involved in the development of cardiac hypertrophy, endothelial dysfunction and even organ damage. ROS contribute to all aspects of cellular function including gene expression, proliferation, migration, and cell death. In our current research, oxidative stress plays an important role in drugs-induced cardiomyopathy. Apoptotic pathways and hypertrophic gene may be involved in the pathogenesis of drug-induced cardiomyopathy. Our new research focus on involvement of NF-kB and AMPK signaling pathways in drugs-induced cardiotoxicity. This will provide important information to understand the molecular mechanisms leading to the development of drug-induced cardiomyopathy which will reveal new therapeutic approaches.
Effects of adrenergic drugs and their blockers on BP 
Effects of drugs on Isolated Rabbit’s Heart
Effect of Nm blockers on Frog Rectus Abdomens  Muscle.