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Departments of 1 Physiology, Cell Biology and 2 Pharmacology, University of Nevada School of Medicine, Reno, Nevada 89557; and 3 Department of Anesthesiology, University of California Davis Medical Center, Sacramento, California 95817
Previous studies suggest that
ether-a-go-go related gene (ERG) KCNH2 potassium channels contribute to
the control of motility patterns in the gastrointestinal tract of
animal models. The present study examines whether these results can be
translated into a role in human gastrointestinal muscles. Messages for
two different variants of the KCNH2 gene were detected: KCNH2 V1 human
ERG (HERG) (28) and KCNH2 V2 (HERGUSO)
(13). The amount of V2 message was greater than V1 in both
human jejunum and brain. The base-pair sequence that gives rise to
domains S3-S5 of the channel was identical to that previously published for human KCNH2 V1 and V2. KCNH2 protein
was detected immunohistochemically in circular and longitudinal smooth
muscle and enteric neurons but not in interstitial cells of Cajal. In
the presence of TTX (10
6 M), atropine (106
M). and L-nitroarginine (104 M) human jejunal
circular muscle strips contracted phasically (9 cycles/min) and
generated slow waves with superimposed spikes. Low concentrations of
the KCNH2 blockers E-4031 (108 M) and MK-499 (3 × 108 M) increased phasic contractile amplitude and the
number of spikes per slow wave. The highest concentration of E-4031
(106 M) produced a 10-20 mV depolarization,
eliminated slow waves, and replaced phasic contractions with a small
tonic contracture. E-4031 (106 M) did not affect
[14C]ACh release from enteric neurons. We conclude that
KCNH2 channels play a fundamental role in the control of motility
patterns in human jejunum through their ability to modulate the
electrical behavior of smooth muscle cells.
membrane potential; smooth muscle; potassium channels; motility; gastrointestinal
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