The use of ryanodine and calcium channel blockers to characterize intra- and extracellular calcium pools mobilized by noradrenaline in the rat vas deferens

1989 ◽  
Vol 165 (2-3) ◽  
pp. 309-313 ◽  
Author(s):  
Gonzalo Vesperinas ◽  
Marion Feddersen ◽  
Jorge Lewin ◽  
J. Pablo Huidobro-Toro
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Vas Deferens ◽  
Extracellular Calcium ◽  
Rat Vas Deferens ◽  
Channel Blockers

Inhibition by calcium channel blockers of the glycogenolytic effect of glucagon in perfused rat liver

1982 ◽  
Vol 99 (4) ◽  
pp. 559-566 ◽  
Author(s):  
Satoshi Kimura ◽  
Toshio Matsumoto ◽  
Ryoko Tada ◽  
Etsuro Ogata ◽  
Kaoru Abe
Keyword(s):  
Cyclic Amp ◽  
Calcium Channel ◽  
Rat Liver ◽  
Calcium Channel Blockers ◽  
Calcium Influx ◽  
Extracellular Calcium ◽  
Channel Blockers ◽  
Perfused Rat Liver ◽  
Glycogenolytic Effect ◽  
Glucose Output

Abstract. Verapamil and diltiazem, calcium channel blockers, inhibited significantly the glucagon-induced glucose output and 45Ca efflux from perfused rat liver at concentrations higher than 50 μm when the perfusate contained calcium. Although the blockers partially interfered with glucagon-induced elevation of cyclic AMP in the tissue, they also inhibited the effects of cyclic AMP. The blockers did not show the inhibitory effects in the absence of perfusate calcium. However, the inhibition of calcium influx into hepatocytes by omission of extracellular calcium or addition of EGTA did not interfere with these effects of glucagon and cyclic AMP. In the presence of extracellular calcium, the blockers did not inhibit cyanide-induced glucose output, indicating that the activity of glycogen phosphorylase and later processes leading to glucose output were not affected by the blockers. These data suggest that, in the presence of calcium, the blockers inhibit the effect of glucagon also at a step (or steps) subsequent to cyclic AMP production and before the activation of phosphorylase b, probably by inhibiting glucagon-induced mobilization of calcium from intracellular calcium pools rather than inhibiting calcium influx into hepatocytes.

Interaction of theophylline, verapamil, and diltiazem on hamster diaphragm muscle force in vitro

1988 ◽  
Vol 254 (3) ◽  
pp. C365-C371 ◽  
Author(s):  
S. A. Esau
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Force Production ◽  
Extracellular Calcium ◽  
Diaphragm Muscle ◽  
Resting Membrane Potential ◽  
Channel Blockers ◽  
Low Frequencies ◽  
High Frequencies

The effect of the calcium channel blocker verapamil (5 microM) or diltiazem (5 microM) on force production and resting membrane potential (Em) was studied in the hamster diaphragm muscle. The calcium channel blockers decreased force at high frequencies of stimulation and decreased Em by 3 +/- 1 mV. The interaction of theophylline and the calcium channel blockers was also studied. When given simultaneously, the calcium channel blockers prevented the increase in force at high frequencies with theophylline at 1 mM and at all frequencies with theophylline at 0.55 mM. There was no change in Em when theophylline and calcium channel blockers were given together. Similar results were obtained by removing external calcium. The decrease in force produced by verapamil was not reversed by subsequent addition of theophylline. Theophylline did reverse the decrease in force produced by diltiazem. Verapamil reversed the increase in force at high frequencies produced by theophylline. Diltiazem reversed the force increase at low frequencies as well. These studies suggest that extracellular calcium is important in skeletal muscle contractility especially at high frequencies. Extracellular calcium is also important for the potentiation of force and the hyperpolarization of the Em produced by theophylline. The mechanism by which extracellular calcium contributes to these actions of theophylline is not known.

Spike aftercurrents in R15 of Aplysia: their relationship to slow inward current and calcium influx

1984 ◽  
Vol 51 (2) ◽  
pp. 387-403 ◽  
Author(s):  
D. V. Lewis
Keyword(s):  
Calcium Channel ◽  
Intracellular Calcium ◽  
Calcium Channel Blockers ◽  
Calcium Influx ◽  
Extracellular Calcium ◽  
Slow Inward Current ◽  
Extracellular Potassium ◽  
Channel Blockers ◽  
Tetraacetic Acid ◽  
Inward Current

Spikes in the bursting neuron, R15, are followed by depolarizing afterpotentials (35) and often by delayed hyperpolarizing afterpotentials as well. Placing the cell in a voltage clamp after a spike allows measurement of the depolarizing aftercurrent (DAC) and hyperpolarizing aftercurrent (HAC) that underlie the afterpotentials. Subthreshold depolarizations give rise to small DACs and HACs. The DAC and the slow inward current (SIC) of R15 are reduced or blocked in a similar manner by many experimental manipulations, e.g., application of dopamine, zero-calcium seawater, zero-sodium seawater, or calcium-channel blockers (Mn2+ and La3+), or cooling the cell from 21-22 degrees C to 10 degrees C. Neither the DAC nor the SIC were blocked by tetrodotoxin (100 uM) and neither was sensitive to altered extracellular potassium. Both the DAC and SIC become larger as the holding potential of the cell is progressively depolarized from -70 to -40 mV. DACs are sensitive to the injection of intracellular calcium chelators (EGTA (ethylene glycol-bis(beta-aminoethyl ether)-N,N1-tetraacetic acid) or EDTA [ethylenedinitrilo)tetraacetic acid]. DAC amplitude is approximately 90% reduced by intracellular EGTA concentration near 1mM. In contrast, the SIC is unchanged or much less affected by the calcium buffers. DACs are also more sensitive to low (1 mM) extracellular calcium than is the SIC. The HAC is also a calcium-dependent current. It is blocked by any experimental manipulation reducing calcium influx or intracellular calcium accumulation, i.e., reduced extracellular calcium, calcium-channel blockers, or intracellular EGTA. We suggest that the DAC and the SIC are carried by the same conductance mechanism. In the case of the DAC, the conductance might be activated by a rise in intracellular calcium activity accompanying the spike and, in the case of the SIC, depolarization per se may be the most important activating condition.

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