scholarly journals ACTIVATION OF AN ELECTROGENIC SODIUM PUMP IN THE SMOOTH MUSCLE CELL MEMBRANE OF GUINEA PIG TAENIA COLI DURING RECOVERY AFTER COLD TREATMENT

1973 ◽  
Vol 23 (1) ◽  
pp. 25-38 ◽  
Author(s):  
Tetsuo MAGARIBUCHI ◽  
Yushi ITO ◽  
Hiroshi KURIYAMA
Keyword(s):  
Smooth Muscle ◽  
Cell Membrane ◽  
Guinea Pig ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Sodium Pump ◽  
Cold Treatment ◽  
Taenia Coli ◽  
Electrogenic Sodium Pump ◽  
Muscle Cell Membrane

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.

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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