© 1995 American Heart Association, Inc.
Articles |
Inhibition and Rapid Recovery of Ca2+ Current During Ca2+ Release From Sarcoplasmic Reticulum in Guinea Pig Ventricular Myocytes
From the Laboratory of Physiology, University of Leuven (Belgium).
Correspondence to K.R. Sipido, Laboratory of Physiology, KUL, Campus Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium.
Abstract We have investigated the modulation of the L-type
Ca2+ channel by Ca2+ released from the
sarcoplasmic reticulum (SR) in single guinea pig ventricular myocytes
under whole-cell voltage clamp. [Ca2+]i was
monitored by fura 2. By use of impermeant monovalent cations in
intracellular and extracellular solutions, the current through
Na+ channels, K+ channels, nonspecific cation
channels, and the Na+-Ca2+ exchanger was
effectively blocked. By altering the amount of Ca2+ loading
of the SR, the time course of the Ca2+ current
(ICa) could be studied during various amplitudes of
Ca2+ release. In the presence of a large Ca2+
release, fast inhibition of ICa occurred, whereas on
relaxation of [Ca2+]i, fast recovery was
observed. The time course of this transient inhibition of
ICa reflected the time course of
[Ca2+]i. However, the inhibition seen in the
first 50 ms, ie, the time of net Ca2+ release from the SR,
exceeded the inhibition observed later during the pulse, suggesting the
existence of a higher [Ca2+] near the channel during this
time. Transient inhibition of ICa during Ca2+
release was observed to a similar degree at all potentials. It could
still be observed in the presence of intracellular ATP-
-S and of
cAMP. Therefore, we conclude that the modulation of ICa by
Ca2+ release from the SR is not related to
dephosphorylation. It could be related to a reduction in the driving
force and to a direct inhibition of the channel by
[Ca2+]i. The observation that the degree of
inhibition does not depend on membrane potential suggests that the
Ca2+ binding site for this modulation is located outside
the pore. The transient nature of the modulation of ICa by
Ca2+ release will contribute to the recovery of
ICa during prolonged action potentials.
Key Words: Ca2+ channel • heart • Ca2+ release • sarcoplasmic reticulum
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