Effects of calcium channel antagonists on the release of prostaglandin e2 from metabolically stressed muscle

Majumdar, Ramanath; Nguyen, Jeffrey T.; Brooke, Michael H.

doi:10.1016/0006-2952(94)90109-0

Cited by 5 publications

(3 citation statements)

References 19 publications

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“…The quantal content of e.p.ps increased in the presence of DNP in a temperature-dependent manner. This effect of DNP might be based, in part, on the stimulation of the influx of Ca2+ ions through voltage-dependent channels in the presence of external Ca2+ ions (Majumdar et al, 1994), as well as on the possible mobilization of Ca2+ ions from internal storage sites, as mentioned above.…”

Section: Discussionmentioning

confidence: 99%

“…Such a blockade is considered to be due to an increase in the concentration of Ca2" ions within the cytoplasm as a result of the release of Ca2" ions from mitochondria (see Erulkar & Fine, 1979). The release of prostaglandin E2 that is induced by DNP in rat skeletal muscle can be abolished by organic calcium antagonists, such as nifedipine and verapamil (Majumdar et al, 1994). These results imply that DNP stimulates the influx of Ca2+ ions through voltage-dependent channels.…”

Section: Introductionmentioning

confidence: 99%

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Dependence on temperature of the effect of dinitrophenol on the release of transmitter quanta at neuromuscular junctions in the mouse diaphragm

Nishimura

Taquahashi

Fujita

et al. 1996

British J Pharmacology

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1 The frequencies (F, s-1) of miniature endplate potentials and the quantal content (m) of endplate potentials were measured intracellularly and simultaneously at mouse diaphragm endplates in a bathing solution that contained 0.6 mM Ca2" ions and 5 mM Mg2" ions.2 Twin pulses at 4 ms intervals gave the quantal contents of the first (ml) and second (m2) responses. The ratio of m2/ml was taken as an indicator of the temporal facilitation of the release of transmitter. 3 Dinitrophenol (DNP, 10 !M) increased the values of F and m at 36'C. This effect did not depend on extracellular Ca" ions.4 The potentiating effect of DNP disappeared at 24°C but the value of m2/ml remained constant. 5 These results suggest that the effect of DNP is modifiable by temperature which can affect systems that control the intracellular metabolism of Ca2" ions.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dependence on temperature of the effect of dinitrophenol on the release of transmitter quanta at neuromuscular junctions in the mouse diaphragm

Nishimura

Taquahashi

Fujita

et al. 1996

British J Pharmacology

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“…K + -Ionen könnten so die Reizschwelle von Nozizeptoren senken und den Schmerz auslösen [56]. Weiter wird berichtet, dass die Erhöhung der intrazellulären Ca 2+ -Konzentration über die Induktion der Cyclooxygenase den Ausstrom des Arachidonsäuremetaboliten und Entzün-dungsmediators Prostaglandin E 2 aus der Muskelzelle verstärkt [49], so dass auch dieser Mechanismus zu einer Sensibilisierung von Nozizeptoren beitragen kann [32]. Anders als in den Extremitäten scheinen diese Abläufe in der Kiefermuskulatur allerdings nicht zwangsläufig mit einer kompletten Erschöpfung des Muskels verbunden zu sein; stattdessen dient der Schmerz hier eher der Vermeidung eines solchen Erschöpfungszustandes [65].…”

Section: Muskelermüdungunclassified

Kiefermuskelschmerz – Neurobiologische Grundlagen

Schindler¹,

Türp

2002

Schmerz

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The masticatory muscles show morphologic, histochemical, electrophysical, and functional features that differ from the other muscles of the body. At least two kinds of masticatory muscle pain should be distinguished: A local pain associated with peripheral mechanical overuse, and a pain associated with changes in the central nociceptive system. Biomechanical factors appear to be important for the first type of muscle pain. Since the typical reaction of a painful muscle consists of inhibition of its activity, traditional concepts that postulate the maintenance of the pain by chronic overuse of the whole muscle are not supported by the current literature. Instead, differential overuse of discrete intramuscular regions appear to provide a more plausible explanation. On the other hand, the possible relationships between functional and structural neuroplastic changes and the second form of chronic muscle pain (e.g., fibromyalgia) still remain speculative.

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Evidence of a temperature-sensitive step in the release of prostaglandin E2 in calcium ionophore-stimulated rat muscle

Majumdar

Gowda

Brooke

1995

Prostaglandins, Leukotrienes and Essential Fatty Acids

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Effects of calcium channel antagonists on the release of prostaglandin e2 from metabolically stressed muscle

Cited by 5 publications

References 19 publications

Dependence on temperature of the effect of dinitrophenol on the release of transmitter quanta at neuromuscular junctions in the mouse diaphragm

Dependence on temperature of the effect of dinitrophenol on the release of transmitter quanta at neuromuscular junctions in the mouse diaphragm

Kiefermuskelschmerz – Neurobiologische Grundlagen

Evidence of a temperature-sensitive step in the release of prostaglandin E2 in calcium ionophore-stimulated rat muscle

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