Yuji Imaizumi (1), Yoshiaki Ohi (1), Hisao Yamamura (1), Susumu Ohya
(2),
Katsuhiko Muraki (2) and Minoru Watanabe (2)
(1) Department of Pharmacology & Therapeutics and (2) Department
of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Nagoya City
University, Nagoya 467-8603, Japan
Abstract: Ca2+ spark is a local and transient Ca2+
release from sarcoplasmic reticulum (SR) through the ryanodine receptor
Ca2+-releasing channel (RyR). In cardiac myocytes, Ca2+
spark is an elementary unit of Ca2+-induced Ca2+ release
(CICR) by opening of RyR(s) in junctional SR (jSR), which is triggered by
Ca2+-influx through L-type Ca2+ channels to the narrow
space between a transverse tubule and jSR. Ca2+ spark has, therefore,
been described as the evidence for "the local control of excitation-contraction
coupling". In contrast, Ca2+ sparks in smooth muscle have
been reported in relation to Ca2+-dependent K+ (KCa)
channel activation and muscle relaxation. A spontaneous Ca2+
spark in a superficial area activates 10 - 100 KCa, channels
nearby and induces membrane hyperpolarization, which reduces Ca2+
channel activity. In several types of smooth muscle cells, which have relatively
high membrane excitability, an action potential (AP) elicits 5 - 20 Ca2+
hot spots (evoked sparks with long life) in the early stage via CICR in
discrete superficial SR elements and activates KCa-channel current
highly responsible for AP repolarization and afterhyperpolarization. CICR
available for contraction may occur more slowly by the propagation of CICR
from superficial SR to deeper ones. The regulatory mechanism of ion channel
activity on plasma membrane by superficial SR via Ca2+ spark
generation in smooth muscle cells may be analogously common in several types
of cells including neurons.
Keywords: Calcium spark, Ryanodine receptor, Cardiac muscle, Smooth muscle,
Potassium channel