The effect of 2-n-propyl-3-dimethylamino-5,6-methylenedioxyindene on caffeine-induced contractures of skeletal muscle

1981 ◽  
Vol 59 (6) ◽  
pp. 617-620 ◽  
Author(s):  
Ralf G. Rahwan ◽  
Michael C. Gerald
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Calcium ◽  
Extracellular Calcium ◽  
Site Of Action ◽  
Isolated Rat

It has been previously postulated that 2-n-propyl-3-dimethylamino-5,6-methylenedioxyindene (pr-MDI) exhibits calcium antagonistic properties with an intracellular site of action. The present investigation further substantiates this hypothesis by providing evidence that pr-MDI inhibits caffeine-induced contractures (which are mediated by intracellular calcium) of the isolated rat hemidiaphragm skeletal muscle both in the presence and in the absence of extracellular calcium.

Sources of calcium mobilized by glucagon in isolated rat hepatocytes

1988 ◽  
Vol 119 (2) ◽  
pp. 301-306 ◽  
Author(s):  
Tetsuya Mine ◽  
Itaru Kojima ◽  
Etsuro Ogata
Keyword(s):  
Angiotensin Ii ◽  
Intracellular Calcium ◽  
Rat Hepatocytes ◽  
Extracellular Calcium ◽  
Transient Increase ◽  
Free Calcium ◽  
Isolated Rat Hepatocytes ◽  
Isolated Rat ◽  
Calcium Pool

Abstract. Effects of glucagon on cytoplasmic concentration of free calcium, [Ca2+]c, were studied in aequorin-loaded hepatocytes. Addition of 5 nmol/l glucagon resulted in a prompt, but transient increase in aequorin bioluminescence. Glucagon, at 5 nmol/l, induced an increase in [Ca2+]c even in medium containing 1 μmol/l calcium, although the response was considerably smaller than that observed in medium containing 1.0 mmol/l calcium. When hepatocytes incubated in the presence of 1 μmol/l extracellular calcium were first stimulated by phenylephrine and subsequently by either glucagon or angiotensin 11, there was a response of [Ca2+]c to glucagon, but not to angiotensin II. Dantrolene (50 μmol/l), which inhibits an increase in [Ca2+]c induced by phenylephrine, did not inhibit the increase in [Ca2+]c induced by glucagon. In contrast, dinitrophenol (50 μmol/l) abolished [Ca2+]c response to glucagon without abolishing the increase in [Ca2+]c induced by angiotensin II. These results suggest that glucagon mobilizes calcium from both intracellular and extracellular pools and that the intracellular calcium pool involved in glucagon action may be different from that mobilized by either phenylephrine or angiotensin II.

Ultra-Rapid Freezing of Isolated Skeletal Muscle Fibers

1977 ◽  
Vol 35 ◽  
pp. 576-577
Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Granular Material ◽  
Nuclear Envelope ◽  
Intracellular Calcium ◽  
Ruthenium Red ◽  
Threshold Concentration ◽  
Rapid Freezing ◽  
Frog Skeletal Muscle ◽  
Electrical Isolation

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.

Nitrendipine blocks high potassium contractures but not twitches in rat skeletal muscle

1988 ◽  
Vol 66 (9) ◽  
pp. 1210-1213 ◽  
Author(s):  
G. B. Frank ◽  
L. Konya ◽  
T. Subrahmanyam Sudha
Keyword(s):  
Skeletal Muscle ◽  
Calcium Ions ◽  
Calcium Uptake ◽  
Channel Blocker ◽  
Mechanical Response ◽  
Extracellular Calcium ◽  
The Other ◽  
Rat Skeletal Muscle ◽  
Potassium Depolarization ◽  
High Potassium

The effects of the organic calcium channel blocker nitrendipine was tested on electrically evoked twitches and on potassium depolarization-induced contractures of rat lumbricalis muscles. Nitrendipine (10−7 to 5 × 10−5 M) blocked only the potassium contractures. It was concluded that blocking calcium uptake through the slow voltage-senstitive calcium channels during potassium depolarization blocks the mechanical response of the muscle. Thus extracellular calcium ions are required for the excitation–contraction (E–C) coupling during depolarization contractures. On the other hand, electrically evoked twitches were not affected by nitrendipine; therefore, extracellular calcium ions entering via the slow voltage-sensitive channels are not required for E–C coupling during the twitch.

Roselle Polyphenols Exert Potent Negative Inotropic Effects via Modulation of Intracellular Calcium Regulatory Channels in Isolated Rat Heart

2016 ◽  
Vol 17 (3) ◽  
pp. 251-259 ◽  
Author(s):  
Yi-Cheng Lim ◽  
Siti Balkis Budin ◽  
Faizah Othman ◽  
Jalifah Latip ◽  
Satirah Zainalabidin
Keyword(s):  
Intracellular Calcium ◽  
Rat Heart ◽  
Isolated Rat Heart ◽  
Inotropic Effects ◽  
Negative Inotropic Effects ◽  
Isolated Rat
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