scholarly journals Dihydropyridine calcium channel antagonists block and agonists potentiate high potassium contractures but not twitches in frog skeletal muscle.

1990 ◽  
Vol 40 (2) ◽  
pp. 205-224 ◽  
Author(s):  
George B. FRANK
1987 ◽  
Vol 164 (3) ◽  
pp. 525-531 ◽  
Author(s):  
Jacques BARHANIN ◽  
Thierry COPPOLA ◽  
Annie SCHMID ◽  
Marc BORSOTTO ◽  
Michel LAZDUNSKI

1994 ◽  
Vol 72 (10) ◽  
pp. 1220-1225 ◽  
Author(s):  
Murat Oz ◽  
George B. Frank

The effects of Bay K8644, a Ca2+ channel agonist, on the mechanical and electrical properties of frog skeletal muscle fibers were investigated. At relatively low concentrations, such as 10−6 and 10−5 M, Bay K8644 significantly potentiated the maximum amplitudes of twitch responses, and this effect was not reversed in the presence of the calcium channel antagonist nitrendipine. At higher concentrations, such as 10−4 M, Bay K8644 depressed the amplitudes of twitch responses, and nitrendipine did not change this effect. At all concentrations, Bay K8644 greatly reduced the area under the tetanic force versus time curve, and this effect was not modified by the concomitant application of Bay K8644 and nitrendipine. Intracellular recordings revealed that the depressing effect of Bay K8644 on tetanic contractions was due to the blockade of sodium action potentials. In conclusion, the present results suggest that the modulation of twitch responses by calcium channel agonist and antagonists, at the concentration range used, is not related to the expected modulation of voltage-sensitive slow calcium channels in frog skeletal muscle fibers, and tetanic contractions are depressed by the calcium channel agonist Bay K8644 through its effect on sodium channels.Key words: Bay K8644, calcium channels, sodium channels, muscle contraction.


Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace

After Howell (1) had shown that ruthenium red treatment of fixed frog skeletal muscle caused collapse of the intermediate cisternae of the sarcoplasmic reticulum (SR), forming a pentalaminate structure by obi iterating the SR lumen, we demonstrated that the phenomenon involves the entire SR including the nuclear envelope and that it also occurs after treatment with other cations, including calcium (2,3,4).From these observations we have formulated a hypothesis which states that intracellular calcium taken up by the SR at the end of contraction causes the M rete to collapse at a certain threshold concentration as the first step in a subsequent centrifugal zippering of the free SR toward the junctional SR (JSR). This would cause a) bulk transport of SR contents, such as calcium and granular material (4) into the JSR and, b) electrical isolation of the free SR from the JSR.


Author(s):  
A. V. Somlyo ◽  
H. Shuman ◽  
A. P. Somlyo

Electron probe analysis of frozen dried cryosections of frog skeletal muscle, rabbit vascular smooth muscle and of isolated, hyperpermeab1 e rabbit cardiac myocytes has been used to determine the composition of the cytoplasm and organelles in the resting state as well as during contraction. The concentration of elements within the organelles reflects the permeabilities of the organelle membranes to the cytoplasmic ions as well as binding sites. The measurements of [Ca] in the sarcoplasmic reticulum (SR) and mitochondria at rest and during contraction, have direct bearing on their role as release and/or storage sites for Ca in situ.


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