Microdetermination of magnesium and calcium in animal tissue

Zusammenfassung Eine Methode zur Bestimmung von 10–40 µg Mg und 5–15 µg Ca in etwa 150 mg Tiergeweben wird beschrieben. Nach Trennung auf Dowex 50-X8 wird Mg mit Komplexon III und Ca mit Na-naphthalohydroxamat bestimmt.     

Effects of calcium and magnesium ions on the frequency of miniature end-plate potential discharges in amphibian muscle in the presence of ethyl alcohol

Zusammenfassung Während bekanntlich Kalzium- und Magnesiumionen keinen Einfluss auf die Frequenz der Spontanrhythmik (m.e.p.p.) der Kaltblütermuskeln in der normalen Ringer-Lösung haben, konnte experimentell festgestellt werden, dass die Frequenz der Spontanrhythmik in einer Äthanol-Ringer-Lösung durch Zusatz von Kalziumionen vermehrt, von Magnesiumionen vermindert wird.     

Unequal distribution of calcium and magnesium of snail neuron

Summary Ca and Mg contents of snail neuron differ depending on the cell type. Ca and Mg near the cell membrane are not equally distributed in the isolated neuron. Ca is almost twice as dense in the axonhillock region than in the cell body. The Mg distribution pattern is the reverse of that of Ca.     

Fluxes of magnesium and calcium during induced activity of frog sartorius muscle

Resumen La representación del influjo de Ca y de Mg en músculo esquelético en reposo de rana as cualtitativamente differente; sin embargo la magnitud de dicho influjo as inicialmente similar. Estímulo mediante pulsos eléctricos o cafeina aumenta significamente el influjo de Ca pero no el de Mg durante un período de 10 min.     

The influence of magnesium and calcium ions on the force produced in rigor muscle

Zusammenfassung Die Rigorspannung glycerinextrahierter Skeletmuskelfasern (Caiman crocodilus) und fibrillärer Insektenflugmuskelfasern (DLM) (L. maximus) konnte durch Zugabe von zweiwertigen Kationen und pH-Erniedrigung reversibel erniedrigt werden sowie durch pH-Erhöhung und Zugabe von Sulfationen erhöht werden. Da unter ähnlichen Bedingungen im Rigor Veränderungen des Abstandes von Aktin- und Myosinfilamenten nachgewiesen wurden^4,5, wurden die beobachteten Spannungsänderungen im Rigor auf Grund neuerer Crossbridgemodelle^3,9 diskutiert.

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We are grateful to Prof. Dr.J. C. Rüegg for helpful suggestions.

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Supported by Deutsche Forschungsgemeinschaft, Grant No. Ru 154/7.     

Calcium and magnesium deficiency-induced atrophy of muscle and calcium accumulation in the spinal cord

After severe dietary calcium-magnesium deficiency in rats, succinic dehydrogenase and acetylcholinesterase enzyme activity of gastrocnemius muscle showed a neurogenic atrophy. This alteration was associated with a high concentration of calcium in the spinal cord.     

Failure of calcium to stimulate Na,K-ATPase in the presence of EDTA

Summary The effect of calcium on Na, K-ATPase activity of rat brain homogenates and its modification by the chelating agent EDTA has been investigated. In the absence of EDTA, free calcium (approximately 10^–6mol/l) stimulates Na,K-ATPase activity; in the presence of EDTA the same concentration of free calcium is without effect on the enzyme. In the absence of EDTA the stimulation by calcium of Na,-K-ATPase activity is enhanced by the additional presence of calmodulin but in the presence of EDTA, even when calmodulin is added to excess, calcium still fails to stimulate the enzyme. The possibility that EDTA interferes with an interaction between a calcium-calmodulin complex and Na,K-ATPase is discussed.The expert technical assistance of Mrs Paula Jarvie is gratefully acknowledged. Thanks are due also to Professor Philip Kuchel for assistance with the calculations to determine the concentrations of metal-ligand complexes in the experimental media.     

Failure of calcium to stimulate Na,K-ATPase in the presence of EDTA

The effect of calcium on Na,K-ATPase activity of rat brain homogenates and its modification by the chelating agent EDTA has been investigated. In the absence of EDTA, free calcium (approximately 10(-6) mol/l) stimulates Na,K-ATPase activity; in the presence of EDTA the same concentration of free calcium is without effect on the enzyme. In the absence of EDTA the stimulation by calcium of Na,K-ATPase activity is enhanced by the additional presence of calmodulin but in the presence of EDTA, even when calmodulin is added to excess, calcium still fails to stimulate the enzyme. The possibility that EDTA interferes with an interaction between a calcium-calmodulin complex and Na,K-ATPase is discussed.     

Sulfhydryl oxidation induces calcium release from fragmented sarcoplasmic reticulum even in the presence of glutathione

Alcian blue and plumbagin induced transient Ca²⁺ release from fragmented sarcoplasmic reticulum. Dithiothreitol (DTT) and glutathione (GSH) partially blocked Ca²⁺ release induced by these oxidizing compounds. Pretreatment of alcian blue and plumbagin with DTT or GSH for more than 1 min was required to abolish the ability of the oxidizing compounds to release Ca²⁺. Mg²⁺ and ruthenium red completely blocked alcian blue-and plumbagin-induced Ca²⁺ release. These results suggest that oxidation of sulfhydryls on Ca²⁺ release channels induces Ca²⁺ release even in the presence of GSH in situ.     

Potassium-induced stimulation of thyrotropin release in vitro. Requirement for presence of calcium and inhibition by thyroxine

Résumé L'augmentation de la concentration en potassium (K⁺) à 25 meq/l et au delà, du liquide dans lequel des hypophyses de rat sont incubées in vitro stimule la sécrétion de l'hormone thyréotrope (TSH). La présence de l'ion calcium (Ca⁺⁺) est nécessaire à cet effet de K⁺; l'incubation dans un milieu sans Ca⁺⁺ empèche l'effet (sécrétion de TSH) de K⁺, qui est rétabli quand on réintroduit Ca⁺⁺ dans le liquide d'incubation. La stimulation de la sécrétion de TSH due à K⁺ est inhibée par la thyroxine. Les effets de K⁺ sur la sécrétion de TSH sont identiques à ceux de TRF (TSH-releasing factor) hypothalamique, en ce qui concerne la présence de Ca⁺⁺ et l'inhibition par la thyroxine.

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Supported by USPHS research grants Nos. AM 08290.04, HD 02577.01, training grant No. GM 956.04; also No. FR 00254 to Common Research Computer Facility, Texas Medical Center. We are pleased to acknowledge the excellent assistance of Mrs.Nancy Pace in the assays involved here.