Modulation of Electrical Properties by Ions, Hormones, and Drugs

Autonomic and Pharmacological Responses of Idiopathic Ventricular Tachycardia Arising from the Left Ventricular Outflow Tract

“…Their common mechanism is thought to be cAMP‐mediated triggered activity 1–3,7 . Adenosine, verapamil, vagal maneuvers, and β‐blockers are known to eliminate RMVT, since they suppress the slow‐inward current directly by modulating the L‐type calcium channel or indirectly by inhibiting production of cellular cAMP 11–14 . VT from LVOT is not so common as that from RVOT, and comprises 10%–18% of whole idiopathic, adenosine‐sensitive VTs 5,7,8 .…”

“…β‐Adrenergic stimulation and catecholamine increase intracellular cAMP production via stimulation of the G s protein and induce various cellular responses including acceleration of the L‐type calcium channel 11,12 . Adenosine activates the inhibitory G i protein via adenosine A 1 receptor stimulation and antagonizes increased cAMP production induced by β‐adrenergic stimulation, resulting in suppression of catecholamine‐stimulated cellular responses 12,13 . Increased cAMP is assumed to cause intracellular calcium overload leading to development of delayed after depolarizations and triggered activity 13 .…”

“…Vagal maneuvers were effective to suppress PVCs of LVOT origin in the present study. Vagal stimulation can inhibit triggered activity through activating G i protein via cardiac muscarinic (M 2 ) receptor to antagonize increased cAMP production induced by catecholamines 12,13 . However, vagal effect alone cannot exclude a mechanism of these PVCs as automatic activity.…”

A Novel Action of Insulin on Cardiac Membrane

“…3 In the heart, insulin regulates various physiological and pathophysiological functions, including myocardial energy metabolism, contractility, protein expression, hypertrophy and cardiomyopathy in diabetes mellitus, and ion transport mechanisms. 3 The actions of insulin on ionic channels and transporters of normal cardiac membrane have been considered to be unremarkable, 4 but recent evidence has been accumulating to indicate the regulatory roles played by insulin on various channels and transporters, eg, stimulation of the L-type Ca 2ϩ current 5,6 and the Na ϩ -Ca 2ϩ exchanger, 7 and upregulation of K ϩ channels. 8 Given that some of these results were obtained at unphysiologically high insulin levels, the actual contribution of each process to physiological function and signal transduction pathways needs careful consideration.…”