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current in smooth
muscle cells of opossum esophagus
Center for Swallowing and Motility Disorders, Brockton/West Roxbury Veterans Affairs Medical Center, West Roxbury 02132; and Harvard Medical School, Boston, Massachusetts 02125
Nitric oxide (NO)
hyperpolarizes visceral smooth muscles. Using the patch-clamp
technique, we investigated the possibility that NO-mediated
hyperpolarization in the circular muscle of opossum esophagus results
from the suppression of a
Ca2+-stimulated
Cl
current. Smooth muscle
cells were dissociated from the circular layer and bathed in
high-K+
Ca2+-EGTA-buffered solution.
Macroscopic ramp currents were recorded from cell-attached patches.
Contaminating K+-channel currents
were blocked with tetrapentylammonium chloride (200 µM) added to all
solutions. Raising bath Ca2+
concentration above 150 nM in the presence of A-23187 (10 µM) activated a leak current
(IL-Ca) with an
EC50 of 1.2 µM at 
100 mV.
The reversal potential
(Erev) of
IL-Ca (8.5 ± 1.8 mV, n = 8) was significantly
different (P < 0.05) from
Erev of the
background current (+4.2 ± 1.2 mV,
n = 8). Equimolar substitution of 135 mM Cl in the pipette
solution with gluconate significantly shifted Erev of
IL-Ca to +16.6 ± 3.4 mV (n = 4)
(P < 0.05 compared with background),
whereas replacement of total Na+
with Tris+ suppressed
IL-Ca but did not
affect Erev
(15 ± 3 mV, n = 3; P > 0.05).
IL-Ca was
inhibited by DIDS (500 µM). Diethylenetriamine-NO adduct (200 µM),
a NO
donor, and 8-bromo-cGMP (200 µM) suppressed IL-Ca by 59 ± 15% (n = 5) and 62 ± 21%
(n = 4) at 100 mV,
respectively. We conclude that in opossum esophageal smooth muscle
NO-mediated hyperpolarization may be produced by suppression of a
Ca2+-stimulated
Cl-permeable conductance
via formation of cGMP.
calcium-activated current; reversal potential; nitric oxide donors; patch clamp; guanosine 3',5'-cyclic monophosphate
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