199 Molecular and Cellular Biochemistry 176: 199–204, 1997. © 1997 Kluwer Academic Publishers. Printed in the Netherlands. Increases of T-type Ca 2+ current in heart cells of the cardiomyopathic hamster Ghassan Bkaily, 1 Adrian Sculptoreanu, 1 Danielle Jacques 1 and Gaétan Jasmin 2 1 Department of Anatomy and Cell Biology, Faculty of Medicine, Université de Sherbrooke, Sherbrooke, Quebec, J1H 5N4; 2 Department of Pathology, Faculty of Medicine, Université de Montréal, Montreal, Quebec, Canada Abstract In the present study, the whole-cell voltage clamp technique was used in order to record the T- and L-type Ca 2+ currents in single heart cells of newborn and young normal and hereditary cardiomyopathic hamsters. Our results showed that the I/V relationship curve as well as the kinetics of the L-type Ca 2+ currents (I Ca(L) ) in both normal and cardiomyopathic heart cells were the same. However, the proportion of myocytes from normal heart hamster that showed L-type I Ca was less than that of heart cells from cardiomyopathic hamster. The I/V relationship curve of the T-type I Ca (I Ca(T) ) was the same in myocytes of both normal and cardiomyopathic hamsters. The main differences between I Ca(T) of cardiomyopathic and normal hamster are a larger window current and the proportion of ventricular myocytes that showed this type of current in cardiomyopathic hamster. The high density of I Ca(T) as well as the large window current and proportion of myocytes showing I Ca(T) may explain in part Ca 2+ overload observed in cardiomyopathic heart cells of the hamster. (Mol Cell Biochem 176: 199–204, 1997) Key words: heart cells, hereditary cardiomyopathy, cardiomyopathy, Ca 2+ currents, T-type Ca 2+ current, L-type Ca 2+ current Address for offprints: G. Bkaily, Department of Anatomy and Cell Biology, Université de Sherbrooke, Faculty of Medicine, Sherbrooke, Quebec, J1H 5N4, Canada Introduction The cardiomyopathy is broadly defined as heart muscle disease. The cardiomyopathy encompasses a wide spectrum of diseases [1–6]. Unfortunately, the cause of many cases of cardiomyopathy in man is unknown or uncertain. The typical idiopathic cardiomyopathy is characterized by heart muscle disease occurring in the absence of hypertension, coronary artery diseases, valvular lesions, congenital cardiac defects, or other recognized forms of heart diseases. These cardio- myopathies may have a congenital or genetic basis. Two extensively studied models of chronic disease are the: (1) cardiomyopathic Syrian hamster and (2) adriamycin cardio- toxicity. Certain generalizations about hypertrophic cardio- myopathy emerged from the currently available data using action potential studies (for review, see refs. [1, 2]). Teneick and Basset [7], using the sucrose gap technique, in fine papillary muscles from normal and pressure overloaded cat hearts showed that the overall time course of the membrane current was qualitatively unchanged by hypertrophy; how- ever, several parameters quantifying the total current and its component parts were altered. The amplitude of the slow Ca 2+ currents was reduced; however, its kinetics did not change and its type was not known at that time. A preventative effect of Ca 2+ blockers such as verapamil, D-600, and diltiazem on the development of the hamster cardiomyopathy was reported [1, 5]. Jasmin et al. [5] reported that the decrease of Ca 2+ load during the development of cardiomyopathy of the hamster by some (but not all) Ca 2+ blockers may suggest that abnor- malities of Ca 2+ channel may play a major role in the increase of [Ca] i in hereditary cardiomyopathy. Also, the same group reported that measurable abnormal changes start to take place in 25–30 day old cardiomyopathic hamsters. In this study, we verified our hypothesis that detectable changes at the mem- brane channel levels may take place before the appearance of measurable abnormalities during the development of cardiomyopathy of the hamster and that Ca 2+ overload in this pathological animal model is not due to an increase of L-type Ca 2+ current.