K201 modulates excitation-contraction coupling and spontaneous Ca2+ release in normal adult rabbit ventricular cardiomyocytes

The drug K201 (JTV-519) increases inotropy and suppresses arrhythmias in failing hearts, but the effects of K201 on normal hearts is unknown. The effect of K201 on excitation-contraction (E-C) coupling in normal myocardium was studied by using voltage-clamp and intracellular Ca(2+) measurements in i...

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Veröffentlicht in:	Cardiovascular research 2007-11, Vol.76 (2), p.236-246
Hauptverfasser:	LOUGHREY, C. M, OTANI, N, SEIDLER, T, CRAIG, M. A, MATSUDA, R, KANEKO, N, SMITH, G. L
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biological and medical sciences Caffeine - pharmacology Calcium - metabolism Cardiac dysrhythmias Cardiology. Vascular system Heart Heart Ventricles - metabolism Humans Medical sciences Myocardial Contraction - drug effects Myocytes, Cardiac - metabolism Rabbits Ryanodine Receptor Calcium Release Channel - physiology Sarcoplasmic Reticulum - metabolism Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism Tacrolimus Binding Proteins - metabolism Thiazepines - pharmacology
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Zusammenfassung:	The drug K201 (JTV-519) increases inotropy and suppresses arrhythmias in failing hearts, but the effects of K201 on normal hearts is unknown. The effect of K201 on excitation-contraction (E-C) coupling in normal myocardium was studied by using voltage-clamp and intracellular Ca(2+) measurements in intact cells. Sarcoplasmic reticulum (SR) function was assessed using permeabilised cardiomyocytes. Acute application of
ISSN:	0008-6363 1755-3245
DOI:	10.1016/j.cardiores.2007.06.014