scholarly journals The Action Potential in the Smooth Muscle of the Guinea Pig Taenia Coli and Ureter Studied by the Double Sucrose-Gap Method

1970 ◽  
Vol 55 (2) ◽  
pp. 147-162 ◽  
Author(s):  
H. Kuriyama ◽  
T. Tomita
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Action Potential ◽  
Membrane Resistance ◽  
Taenia Coli ◽  
Free Solution ◽  
Ureter Replacement ◽  
A Cell ◽  
Sucrose Gap ◽  
Electrotonic Potential

The configuration of the electrotonic potential and the action potential observed by the double sucrose-gap method was similar to that observed with a microelectrode inserted into a cell in the center pool between the gaps. In the taenia and the ureter, the evoked spike was larger in low Na or in Na-free (sucrose substitute) solution than in normal solution. However, the plateau component in the ureter was suppressed in the absence of Na. In Ca-free solution containing Mg (3–5 mM) and Na (137 mM), the membrane potential and membrane resistance were normal, but no spike could be elicited in both the taenia and ureter. Replacement of Ca with Sr did not affect the spike in the taenia, nor the spike component of the ureter but prolonged the plateau component. The prolonged plateau disappeared on removal of Na, while repetitive spikes could still be evoked. It was concluded that the spike activity in the taenia and in the ureter of the guinea pig is due to Ca entry, that the plateau component in the ureter is due to an increase in the Na conductance of the membrane, and that both mechanisms, for the spike and for the plateau, are separately controlled by Ca bound in the membrane.

Calcium requirement for the α-action of catecholamines on guinea-pig taenia coli

1977 ◽  
Vol 197 (1128) ◽  
pp. 271-284 ◽  
Keyword(s):  
Guinea Pig ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Taenia Coli ◽  
Free Solution ◽  
Normal Concentration ◽  
Calcium Requirement ◽  
Inner Surface ◽  
Sucrose Gap ◽  
Na Ions

The effect of removal and readmission of Ca 2+ on the response of guinea-pig taenia coli to the α-action of adrenaline and noradrenaline, i. e. hyperpolarization and decrease in membrane resistance, was studied with the double sucrose-gap method. The depolarization and reduction of membrane resistance caused by Ca removal were prevented by raising the external Mg concentration, since it was found that high Mg 2+ , up to complete substitution of the external Na + with Mg 2+ (93 mM Mg), did not significantly modify the effect of adrenaline in the presence of the normal concentration of Ca 2+ (2.5 mM). In Ca-free solution containing 124 mM Na, 12 mM Mg and 0.5 mM EGTA, the adrenaline effect gradually disappeared within 10-20 min. The recovery of the adrenaline effect was usually complete within 5 min after readmission of 2.5 mM Ca. When the external Na + was low or absent and Mg 2+ was high, it was more difficult to abolish the response to adrenaline by removal of Ca. Furthermore, restoration of the normal external Ca concentration in the presence of low Na and high Mg produced slow and incomplete recovery of the response to adrenaline. A brief transient application of Ca (5 mm for 15-30 s) to a muscle superfused with Ca-free solution, produced hyperpolarization and increase in membrane resistance. However, a similar Ca application in Ca-free solution containing adrenaline, caused hyperpolarization with a reduction of membrane resistance. The efficacy of Ca, causing hyperpolarization associated with a reduction of membrane resistance in the presence of adrenaline, was stronger when the external Na concentration was high and the Mg concentration was low than in the presence of high Mg and low or 0 Na. It wras concluded that the presence of Ca is essential for the hyper-polarization and the increase in membrane conductance caused by adrenaline, and that the site of Ca involvement is probably at the inner surface of the membrane. Mg and Na ions may affect the response to adrenaline through modification of the amount of Ca at the strategic site, by influencing the Ca movement across the membrane.

Endogenous prostaglandin in guinea pig taenia coli

1976 ◽  
Vol 230 (1) ◽  
pp. 149-157 ◽  
Author(s):  
T Yamaguchi ◽  
B Hitzig ◽  
RF Coburn
Keyword(s):  
Guinea Pig ◽  
Surface Membrane ◽  
Membrane Resistance ◽  
Threshold Concentration ◽  
Mechanical Activity ◽  
Taenia Coli ◽  
Endogenous Prostaglandin ◽  
Sucrose Gap ◽  
Spontaneous Action ◽  
Spontaneous Action Potentials

Prostaglandin (PGE) is synthesized in the guinea pig taenia coli. A low threshold concentration for an effect of exogenous PGE1 or PGE2 on spontaneous mechanical activity was demonstrated. The PG synthetase inhibitors aspirin, indomethacin, and 5,8,11,14-eicosatetraynoic acid, at concentrations that inhibited PGE efflux, had effects on spontaneous mechanical activity, membrane potential, membrane resistance, and evoked and spontaneous action potentials (single and double sucrose-gap methods) that were consistent with an action due to inhibition of membrane PGE concentration. The threshold concentration of indomethacin, which inhibited PGE efflux, was the same as the concentration that inhibited spontaneous mechanical activity. Pretreatment with ouabain (10(-6)-10(-5) g/ml) or elevated extracellular K+ (29 and 126 mM) made the guinea pig taenia coli entirely refractory to exogenous PGE1 or PGE2; the mechanical effects of the three prostaglandin synthetase inhibitors also were absent in the presence of elevated K+ or ouabain. The data are consistent with a hypothesis that, under conditions of our experiments, endogenous PGE has an effect on resting tension and spontaneous mechanical activity and on properties of the surface membrane of the guinea pig taenia coli.

Confirmation of conductance increase by adrenalin in the guinea-pig taenia coli (α-action)

1977 ◽  
Vol 198 (1133) ◽  
pp. 473-477 ◽  
Keyword(s):  
Guinea Pig ◽  
Time Constant ◽  
Membrane Resistance ◽  
Taenia Coli ◽  
Frequency Range ◽  
Tissue Impedance ◽  
Membrane Capacity ◽  
Sucrose Gap ◽  
Conductance Increase ◽  
Sinusoidal Currents

In the guinea-pig taenia coli, adrenalin hyperpolarized the membrane and decreased the amplitude of electrotonic potentials when recorded with micro electrodes from the centre pool (500 μm in width) of the double sucrose-gap apparatus. The reduction of the time constant of electrotonic potentials was proportional to that of the amplitude, indicating that the membrane capacity remained constant. The tissue impedance, measured by sinusoidal currents with a frequency range of 0.1–50 Hz, also indicated that the decrease of membrane resistance by adrenalin was accompanied by little change in the membrane capacity.

Increase of membrane conductance by adrenaline in the smooth muscle of guinea-pig taenia coli

1969 ◽  
Vol 172 (1027) ◽  
pp. 89-102 ◽  
Keyword(s):  
Smooth Muscle ◽  
Potassium Concentration ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Taenia Coli ◽  
High Potassium ◽  
External Potassium ◽  
Sucrose Gap ◽  
Muscle Cell Membrane

(1) The double sucrose-gap method was used to record changes in membrane resistance in intestinal smooth muscle strips. (2) Adrenaline reduced the membrane resistance; it hyperpolarized the membrane and blocked spontaneous and evoked spikes. (3) When the membrane potential was shifted by applying conditioning current, the hyperpolarization produced by adrenaline was larger during depolarization and smaller during hyperpolarization. The hyperpolarization caused by adrenaline was converted into depolarization by 18 to 20 mV conditioning hyperpolarization. (4) The resting membrane resistance was increased in the absence of potassium and in low external chloride (replaced with benzene- or ethane-sulphonate); it was decreased by excess potassium and by nitrate substitution for chloride. (5) The reduction of the membrane resistance by adrenaline was potentiated by high external potassium and by replacement of chloride with nitrate; it was diminished by low external potassium and by replacement of chloride with benzene- or ethane-sulphonate. (6) The hyperpolarization by adrenaline was reduced by raising the external potassium concentration; it was increased by lowering the external potassium concentration. In a solution containing low chloride and high potassium (24 m M ), adrenaline often produced depolarization. (7) It was concluded that adrenaline increases mainly the potassium conductance and also the chloride conductance of the smooth muscle cell membrane. Sodium seemed to be less important for the adrenaline action.

The α-action of catecholamines on the guinea-pig taenia coli in K-free and Na-free solution and in the presence of ouabain

1977 ◽  
Vol 197 (1128) ◽  
pp. 255-269 ◽  
Keyword(s):  
Guinea Pig ◽  
Prolonged Exposure ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Equilibrium Potential ◽  
Taenia Coli ◽  
Free Solution ◽  
Na Pump ◽  
K Concentration ◽  
External K

The responses of guinea-pig taenia coli to the α-action of adrenaline and noradrenaline, recorded with the double sucrose-gap method, were ( a ) studied in conditions which inhibit Na-pump activity (exposure to 0 K, 0 Na, ouabain, low temperature) and ( b ) compared with the effect of Na-pump activation (readmission of K after prolonged exposure to 0 K). When the external K concentration was modified, the alteration of the change in membrane potential produced by the catecholamines was as would be expected from the shift of the K-equilibrium potential. The decrease in the membrane resistance was greater in a high external K con­centration and smaller in K-free solution. Readmission of K after prolonged exposure to K-free solution produced a large hyperpolarization, but, in the presence of ouabain (5 × 10 -5 M) or in the absence of Na, K readmission produced depolarization. In contrast, the effects of adrenaline and noradrenaline were not essentially modified by ouabain, nor by removal of Na. Reduction of the external K concentration enhanced the hyperpolarization by catecholamines even in the presence of ouabain or in the absence of external Na. During prolonged exposure to adrenaline or noradrenaline (7min) the increase in membrane conductance and the hyperpolarization of the membrane were largely maintained, though there was some spontaneous recovery in the presence of the catecholamines. These long-lasting respon­ses were essentially the same when the temperature was lowered from 37 to 20°C, and also in the presence of ouabain. All the results obtained were unaffected by the presence or absence of propranolol. It was concluded that the hyperpolarization produced by the α-action of catecholamines did not involve an activation of the Na-pump but was mainly caused by an increase in the K conductance of the membrane.

Mechanism of alpha-adrenergic excitation in bovine lymphatic smooth muscle

1987 ◽  
Vol 252 (5) ◽  
pp. H873-H878 ◽  
Author(s):  
N. G. McHale ◽  
J. M. Allen ◽  
H. L. Iggulden
Keyword(s):  
Smooth Muscle ◽  
Action Potential ◽  
Safety Margin ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Constant Current ◽  
Beta Blockade ◽  
Gap Technique ◽  
Alpha Receptors ◽  
Sucrose Gap

Measurements were made, using the double sucrose-gap technique, of electrical and mechanical responses of bovine lymphatic smooth muscle to constant current pulses. After beta-blockade with 10(-6) M propranolol, stimulation of the alpha-receptors with norepinephrine (5 X 10(-6) M) depolarized the membrane and decreased membrane conductance. The depolarization and decrease in membrane conductance persisted in Li+- and choline-substituted low-Na+ solution, in methanesulfonate-substituted low-Cl- solution, and in Ca2+- free solution containing 1 mM ethyleneglycol-bis(beta-aminoethylether)-N, N'-tetraacetic acid. Tetraethylammonium (10 mM) did not itself affect membrane resistance nor did it block the increase in resistance due to norepinephrine. In contrast, cesium (10 mM) increased membrane resistance and prevented norepinephrine from increasing this further. As well as these effects on membrane resistance, norepinephrine (5 X 10(-6) M) increased the duration of the action potential, and this was accompanied by an increased force of contraction. Tetraethylammonium prolonged the action-potential plateau and potentiated norepinephrine's effect. These results suggest that norepinephrine is likely to increase the efficiency of lymphatic pumping due to both its positive inotropic effect and the improved safety margin for propagation resulting from the increase in membrane resistance. The latter effect may be due to the suppression of an outward K+ current.

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