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channels and MLCK in slow IJP in opossum esophageal smooth
muscle
Gastrointestinal Disease Research Unit and Departments of Medicine, Biology, and Physiology, Queen's University, Kingston, Ontario, Canada K7L 5G2
The possible
contribution of Ca2+-activated Cl
channel
[ICl(Ca)] and myosin light-chain kinase (MLCK) to
nonadrenergic, noncholinergic slow inhibitory junction potentials
(sIJP) was studied using conventional intracellular microelectrode
recordings in circular smooth muscle of opossum esophageal body and
guinea pig ileum perfused with Krebs solution containing atropine (3 µM), guanethidine (3 µM), and substance P (1 µM). In opossum
esophageal circular smooth muscle, resting membrane potential (MP) was
51.9 ± 0.7 mV (n = 89) with MP fluctuations of
1-3 mV. A single square-wave nerve stimulation of 0.5 ms duration and
80 V induced a sIJP with amplitude of 6.3 ± 0.2 mV,
half-amplitude duration of 635 ± 19 ms, and rebound depolarization amplitude of 2.4 ± 0.1 mV (n = 89). 9-Anthroic acid (A-9-C), niflumic acid (NFA), wortmannin, and
1-(5-chloronaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine (ML-9)
abolished MP fluctuations, sIJP, and rebound depolarization in a
concentration-dependent manner. A-9-C and NFA but not wortmannin and
ML-9 hyperpolarized MP. In guinea pig ileal circular smooth muscle,
nerve stimulation elicited an IJP composed of both fast (fIJP) and slow
(sIJP) components, followed by rebound depolarization. NFA (200 µM)
abolished sIJP and rebound depolarization but left the fIJP intact.
These data suggest that in the tissues studied, activation of
ICl(Ca), which requires MLCK, contributes to resting MP,
and that closing of ICl(Ca) is responsible for sIJP.
nitric oxide; niflumic acid; wortmannin; intracellular microelectrode recording
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