Direct Measurement of L‐Type Ca2+Window Current in Heart Cells
作者:
Yuji Hirano,
Adriana Moscucci,
Craig January,
期刊:
Circulation Research
(OVID Available online 1992)
卷期:
Volume 70,
issue 3
页码: 445-455
ISSN:0009-7330
年代: 1992
出版商: OVID
关键词: Ca2+current;activation;inactivation;window current;Purkinje cells;heart
数据来源: OVID
摘要:
The activation and inactivation relations of several ion channel currents overlap, suggesting the existence of a steady-state or “window” current. We studied L-type Ca2+channel window current in single cardiac Purkinje cells using a voltage-clamp protocol by which channels were first inactivated nearly completely during a long-duration depolarizing step, and then the recovery of Ca2+current was observed during repolarizing steps into the L-type Ca2+window voltage range. With these conditions, a small-amplitude inward Ca2+current gradually developed after repolarization to voltages within the window but not after steps to voltages positive or negative to it. Window current was suppressed by Cd2+(50 μM), nifedipine (1 μM), and nicardipine (1 μM), and it was augmented by isoproterenol (5 μM) and Bay K 8644 (1 μM). At voltages at which window current developed, L-type Ca2+channels also recovered to a closed state from which they could be reopened by an additional depolarizing step. At voltages positive to the window range, channel recovery to a closed state(s) was absent, whereas at voltages negative to the window range, channel recovery to a closed state(s) increased, as expected from the “steady-state” inactivation relation. Our results provide direct measurement of L-type Ca2+window current and distinguish it from other processes, such as slow inactivation. Our findings support the postulate that within a window there occur channel transitions from inactivated to closed states, and these channels (re)open, and this process may occur repetitively. Some physiological and pathophysiological roles for L-type Ca2+window current are discussed. (Circulation Research1992;70:445–455)
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