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Asthma Research Group, Firestone Institute for Respiratory Health, St. Joseph's Hospital; and Department of Medicine, McMaster University, Hamilton, Ontario, Canada L8N 4A6
In general,
excitation-contraction coupling in muscle is dependent on
membrane depolarization and hyperpolarization to regulate the opening
of voltage-dependent Ca2+ channels and, thereby, influence
intracellular Ca2+ concentration
([Ca2+]i). Thus Ca2+ channel
blockers and K+ channel openers are important tools in the
arsenals against hypertension, stroke, and myocardial infarction, etc.
Airway smooth muscle (ASM) also exhibits robust Ca2+,
K+, and Cl
currents, and there are elaborate
signaling pathways that regulate them. It is easy, then, to presume
that these also play a central role in contraction/relaxation of ASM.
However, several lines of evidence speak to the contrary. Also, too
many researchers in the ASM field view the sarcoplasmic reticulum as
being centrally located and displacing its contents uniformly
throughout the cell, and they have focused almost exclusively on the
initial single [Ca2+] spike evoked by excitatory
agonists. Several recent studies have revealed complex spatial and
temporal heterogeneity in [Ca2+]i, the
significance of which is only just beginning to be appreciated. In this
review, we will compare what is known about ion channels in ASM
with what is believed to be their roles in ASM physiology. Also, we
will examine some novel ionic mechanisms in the context of
Ca2+ handling and excitation-contraction coupling in ASM.
excitation-contraction coupling; ion channels; membrane potential
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