scholarly journals Caffeine and Excitation-Contraction Coupling in the Guinea Pig Taenia Coli

1971 ◽  
Vol 57 (4) ◽  
pp. 448-463 ◽  
Author(s):  
Y. Ito ◽  
H. Kuriyama

The effects of caffeine (0.2–10 mM) on the electrical and mechanical activities of guinea pig taenia coli were investigated with the double sucrose-gap method. Caffeine evoked a small tension with a latency of 20–30 sec, then phasic contraction developed and finally relaxation. The initial tension development also appeared in the Na-free solution without any marked changes in the membrane potential and membrane resistance. The phasic contraction disappeared in the Na-free solution. The relaxation in the presence of caffeine was accompanied by depolarization block of the spike generation. The minimum concentration of Ca ion needed to evoke the tension development by the caffeine was 10-7 M. Caffeine also potentiated the twitch tension below a concentration of 5 mM either in the Na-free solution or at low temperature (5°C). NO3- and Br- showed a similar response to caffeine on the potentiation of the twitch tension at low temperature.

1970 ◽  
Vol 55 (2) ◽  
pp. 147-162 ◽  
Author(s):  
H. Kuriyama ◽  
T. Tomita

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.


1977 ◽  
Vol 197 (1128) ◽  
pp. 255-269 ◽  

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.


1977 ◽  
Vol 197 (1128) ◽  
pp. 271-284 ◽  

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.


1994 ◽  
Vol 266 (4) ◽  
pp. H1422-H1433 ◽  
Author(s):  
A. J. Levi ◽  
K. W. Spitzer ◽  
O. Kohmoto ◽  
J. H. Bridge

In mammalian heart muscle, Ca entry through L-type Ca channels is thought to be the primary trigger for the sarcoplasmic reticulum (SR) Ca release, which initiates contraction. The results of this study show that, in guinea pig myocytes with a normal internal Na (10 mM Na in pipette), another trigger mechanisms for SR release and contraction exists. A crucial feature of these experiments was the ability to change rapidly the extracellular environment of a single myocyte so that alterations of intracellular Ca and SR Ca load were minimized for each solution change. We found the following results. 1) A switch to Na-free solution 50 ms before depolarization led to an increase of phasic contraction without increasing L-type Ca current (Ica) or Ca loading of the SR. 2) Although rapid application of 20 microM nifedipine 3 s before a + 10-mV pulse blocked ICa completely, 43 +/- 11 (SE) % of the phasic contraction remained. Similar results were obtained by rapid switching to 150 microM Cd to block ICa. 3) Phasic contraction and ICa had different voltage dependence. With steps to positive potentials there was little ICa but still a substantial phasic contraction. 4) Under action potential conditions, 64.6 +/- 7.9% of the control phasic contraction remained after switching to 20 microM nifedipine to block ICa. 5) The contraction remaining with nifedipine was unaffected by adding 100 microM Ni. Because 100 microM Ni blocks T-type Ca channels, this shows that Ca entry via T-type Ca channels is not involved in triggering SR release. 6) The phasic contraction remaining after a rapid switch to nifedipine was blocked completely by adding 5 mM Ni. Because this concentration of Ni is known to block the Na-Ca exchange, this result suggests that the exchange plays a role in triggering SR release. Taken together, the present results indicate that depolarization-induced Ca entry on the Na-Ca exchange is able to trigger SR release and phasic contraction. This explanation can account for increased phasic contraction after a rapid switch to Na-free solution, persistence of a phasic contraction in the complete absence of ICa, substantial phasic contraction at positive test potentials where there is no ICa, and abolition of nifedipine-resistant contraction by 5 mM Ni.


1976 ◽  
Vol 230 (1) ◽  
pp. 149-157 ◽  
Author(s):  
T Yamaguchi ◽  
B Hitzig ◽  
RF Coburn

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.


1978 ◽  
Vol 50 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Hiroshi Ozaki ◽  
Yukisato Ishida ◽  
Norimoto Urakawa
Keyword(s):  

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