scholarly journals RESPONSES TO FIELD STIMULATION OF THE SMOOTH MUSCLE CELL MEMBRANE OF THE GUINEA PIG STOMACH

1975 ◽  
Vol 25 (3) ◽  
pp. 333-344 ◽  
Author(s):  
Yushi ITO ◽  
Hirosi KURIYAMA
Keyword(s):  
Smooth Muscle ◽  
Cell Membrane ◽  
Guinea Pig ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Field Stimulation ◽  
Guinea Pig Stomach ◽  
Stimulation Of ◽  
Muscle Cell Membrane

Electrical properties of smooth muscle cell membrane of opossum esophagus

1985 ◽  
Vol 248 (3) ◽  
pp. G342-G346 ◽  
Author(s):  
M. S. Kannan ◽  
L. P. Jager ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Electrical Properties ◽  
Cell Membrane ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Smooth Muscles ◽  
Mechanical Activity ◽  
Circular Smooth Muscle ◽  
Stimulation Of ◽  
Muscle Cell Membrane

The electrical properties of the circular smooth muscle layer from the North American opossum esophagus (body) were studied in vitro by microelectrode recording techniques, both at rest and during stimulation of intramural inhibitory nerves. All observations were made at 37 degrees C in an Abe-Tomita partitioned bath on muscle strips dissected 2 cm orad of the lower esophageal sphincter. At rest, the potential of the smooth muscle cell membrane was -49 +/- 4 mV (mean +/- SE); the length constant and the time constant were 2.0 +/- 0.6 mm and 120 +/- 16 ms, respectively. The inhibitory junction potential (IJP) elicited by stimulation of intramural nerves was followed by a "rebound" or "off" response, characterized by a membrane depolarization on which spikes were superimposed and concomitant mechanical activity of the preparation that usually caused dislocation of the recording microelectrode. The maximal IJP amplitude was 35 mV, and the response reversed at a membrane polarization to -90 mV, suggesting that the IJP was due to an increase of the permeability toward potassium ions. The invariability of the IJP latency at different distances from the stimulating electrodes (1.25-4 mm) suggests that the latency is largely due to diffusion of transmitter from nerve varicosities to postsynaptic receptor sites. Depending on the rate, prolonged stimulation caused fusion of IJP or a continuous hyperpolarization of the membrane. The hyperpolarization faded with time, but off responses were only observed after terminating stimulation. The passive electrical properties of the membrane are comparable with those of other gastrointestinal smooth muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Unusual potassium channels mediate nonadrenergic noncholinergic nerve-mediated inhibition in opossum esophagus

1985 ◽  
Vol 63 (2) ◽  
pp. 107-112 ◽  
Author(s):  
J. Jury ◽  
L. P. Jager ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Guinea Pig ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Membrane Resistance ◽  
Potassium Ion ◽  
Ion Permeability ◽  
Muscle Cell Membrane

Field stimulation of the circular muscle of the opossum esophagus produces a transient hyperpolarization (inhibitory junction potential, IJP) followed by an "off" depolarization. A similar nonadrenergic, noncholinergic (NANC) response in guinea pig taenia caecum has been shown to be due to an increase in the potassium ion permeability of the smooth muscle cell membrane. Double sucrose gap studies showed a decrease in resistance during the IJP, and a reversal at an estimated membrane potential of about −90 mV (4 mM K+). The reversal potential was dependent on the extracellular potassium concentration, shifting to −75 mV when the potassium in the superfusion medium was increased to 10 mM. The IJP in the opossum esophageal circular smooth muscle is therefore like the IJP of the guinea pig taenia caecum in that it is probably due to a selective increase in potassium ion permeability. Potassium conductance blocking agents, tetraethylammonium chloride (TEA, 20 mM) and 4-aminopyridine (4-AP, 5 mM) both caused a depolarization of the smooth muscle cell membrane, but TEA increased the membrane resistance, whereas 4-AP did not affect the membrane conductance in a consistent way. A decrease in IJP amplitude owing to these agents was not apparent. Apamin (10 μM) did not affect the membrane potential, the membrane resistance, or the IJP. Quinine (0.1 mM) produced effects quantitatively similar to those of TEA. Quinine (1 mM) did abolish the IJP, however, this was likely due to a blockade of impulse transmission of the intramural nerves. These results suggest that the receptor-operated channels opened by the NANC-nerve mediator in this tissue are unusual in that they are different from those functioning to maintain the resting membrane potential and they differ from those involved in the IJP in the guinea pig taenia caecum.

Characterization of inhibitory innervation in porcine colonic circular muscle

1988 ◽  
Vol 66 (11) ◽  
pp. 1386-1397 ◽  
Author(s):  
L. P. Jager ◽  
M. W. G. Van Der Schaar
Keyword(s):  
Smooth Muscle ◽  
Cell Membrane ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Elevated Temperatures ◽  
Circular Muscle ◽  
Membrane Resistance ◽  
Circular Smooth Muscle ◽  
Stimulation Of ◽  
Muscle Cell Membrane

Effects of stimulation of intramural nerves in the circular smooth muscle layer of the porcine colon (Sus scrofa domestica) were studied using the sucrose-gap technique. Electrical field stimulation of the preparation, superfused with Krebs solution at 21 °C, induced a transient hyperpolarization of the smooth muscle cell membrane. This hyperpolarization was an inhibitory junction potential (IJP). The responses obtained from circular muscle originating from either the centripetal or centrifugal gyri of the ascending colon did not differ significantly. The UP was characterized as being mediated by intramural, nonadrenergic, noncholinergic (NANC) nerves. The amplitude and latency of the IJP changed linearly with temperature (15–25 °C: +1 mV and −0.1 s per degree Celsius, respectively) reflecting a temperature-dependent synchronization of transmitter release. The membrane resistance decreased during the IJP. The IJP amplitude decreased or increased during conditioning hyperpolarizations or depolarizations, respectively, and reversed at membrane potentials about 30 mV more negative than the resting membrane potential. Potassium conductance blocking agents, barium (1 mM), tetraethylammonium chloride (TEA, 20 mM), 4-aminopyridine (4-AP, 5 mM), apamin (1 μM), and aminacrine (10−4 M) added to the superfusion medium increased the membrane resistance. Only barium, TEA, and apamin depolarized the smooth muscle cell membrane. The IJP amplitude decreased in the presence of aminacrine and apamin to 75 and 35%, respectively, suggesting that apamin-sensitive Ca2+-activated K+ channels are involved in this response. ATP, adenosine, and related adenine nucleotides in concentrations up to 10−3 M did not mimic the IJP. Superfusion with ATP for 15 min revealed a gradually increasing attenuation by up to 20% of the IJP. This might suggest that the release of neurotransmitter from intramural NANC nerves is modulated presynaptically via purinoceptors. Exogenously applied vasoactive intestinal polypeptide (VIP) in concentrations of 10−9 to10−4 M did not affect the preparation. Also at elevated temperatures (up to 35 °C), VIP (10−7 to 10−4 M) did not cause measurable effects. It is concluded that the inhibitory mediator of the intramural NANC nerves present in the circular muscle layers of the porcine colon is neither a purine nor VIP.

Voltage-gated K+ channels at an early stage of chronic hypoxia-induced pulmonary hypertension in newborn piglets

2006 ◽  
Vol 291 (6) ◽  
pp. L1169-L1176 ◽  
Author(s):  
Candice D. Fike ◽  
Mark R. Kaplowitz ◽  
Yongmei Zhang ◽  
Jane A. Madden
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Cell Membrane ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Chronic Hypoxia ◽  
Early Stage ◽  
Membrane Properties ◽  
Voltage Gated ◽  
Muscle Cell Membrane

Our purpose was to determine whether smooth muscle cell membrane properties are altered in small pulmonary arteries (SPA) of piglets at an early stage of pulmonary hypertension. Piglets were raised in either room air (control) or hypoxia for 3 days. A microelectrode technique was used to measure smooth muscle cell membrane potential ( Em) in cannulated, pressurized SPA (100- to 300-μm diameter). SPA responses to the voltage-gated K+ (KV) channel antagonist 4-aminopyridine (4-AP) and the KV1 family channel antagonist correolide were measured. Other SPA were used to assess amounts of KV1.2, KV1.5, and KV2.1 (immunoblot technique). Em was more positive in SPA of chronically hypoxic piglets than in SPA of comparable-age control piglets. The magnitude of constriction elicited by either 4-AP or correolide was diminished in SPA from hypoxic piglets. Abundances of KV1.2 were reduced, whereas abundances of both KV1.5 and KV2.1 were unaltered, in SPA from hypoxic piglets. At least partly because of reduced amounts of KV1.2, smooth muscle cell membrane properties are altered such that Em is depolarized and KV channel family function is impaired in SPA of piglets at an early stage of chronic hypoxia-induced pulmonary hypertension.

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