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AJP - Heart and Circulatory Physiology, Vol 259, Issue 6 1842-H1850, Copyright © 1990 by American Physiological Society
ARTICLES |
J. Y. Wu and S. L. Lipsius
Department of Physiology, Stritch School of Medicine, Loyola University of Chicago, Maywood, Illinois 60153.
Whole cell voltage-clamp techniques were used to study the effects of extracellular Mg2+ on T- and L-type Ca2+ currents recorded from single atrial myocytes from cat heart. T and L currents were distinguished primarily by their voltage dependence. With 5.4 mM Ca2+ as charge carrier, maximal T- and L-current densities were 1.0 +/- 0.06 and 9.7 +/- 0.4 pA/pF, respectively. Nickel (Ni2+, 50 microM) inhibited maximal T current (-65.6 +/- 5.9%) more than L current (-15.7 +/- 2.4%), and 10 microM cadmium (Cd2+) inhibited L current (-65.5 +/- 5.9%) without significant effect on T current (-8.7 +/- 8.1%). Mg2+ elicited a dose-dependent inhibition of both T and L currents. Mg2+ less than 8.4 mM inhibited T current more than L current. At Mg2+ greater than or equal to 8.4 mM, T-current inhibition reach a plateau at approximately 52%, whereas L current was further inhibited (-65%) at 16.8 mM Mg2+. Mg2+ elicited a dose-dependent positive shift in half-maximal voltages of activation and inactivation for both T and L currents. Mg2(+)-induced inhibition of both T and L currents was greater in lower (2.7 mM) external Ca2+. Finally, 4.2 mM Mg2+ and 50 microM Ni2+ elicited a similar decrease in the late diastolic slope of subsidiary pacemaker action potentials, whereas 10 microM Cd2+ markedly inhibited action potential amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)
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