A calcium-induced calcium release mechanism mediated by calsequestrin

2008 ◽  
Vol 253 (4) ◽  
pp. 668-679 ◽  
Author(s):  
Young-Seon Lee ◽  
James P. Keener
Keyword(s):  
Calcium Release ◽  
Release Mechanism ◽  
Calcium Induced Calcium Release

scholarly journals Calcium-induced calcium release mechanism in guinea pig taenia caeci.

1989 ◽  
Vol 94 (2) ◽  
pp. 363-383 ◽  
Author(s):  
M Iino
Keyword(s):  
Guinea Pig ◽  
Calcium Release ◽  
Adenine Nucleotide ◽  
Physiological Role ◽  
Release Mechanism ◽  
Smooth Muscle Fiber ◽  
Skinned Smooth Muscle ◽  
Intracellular Ca ◽  
Almost All ◽  
Calcium Induced Calcium Release

Fura-2 was used to measure the amount of Ca released from the intracellular Ca store of a saponin-skinned smooth muscle fiber bundle of the guinea pig taenia caeci (width, 150-250 microns) placed in a capillary cuvette at 20-22 degrees C. The amount of Ca actively loaded into the store was assayed when released by the application of 50 mM caffeine and/or 10 microM inositol 1,4,5-trisphosphate (IP3) in the absence of ATP, and was found to have a biphasic dependence on the loading [Ca2+] with a peak near pCa 6. After Ca loading at pCa 6, IP3 released almost all the releasable Ca, whereas caffeine discharged Ca from only approximately 40% of the store. The maximum amount of Ca in the store was some 220 mumol/liter cell water. Ca in the caffeine-releasable store was released approximately exponentially to zero with time when Ca2+ was applied in the absence of ATP, and the rate constant of the Ca-induced Ca release (CICR) increased steeply with the concentration of Ca2+ applied. Increase in [Mg2+] (0.5-5.0 mM) or decrease in pH (7.3-6.7) shifted the relation between pCa and the rate of CICR roughly in parallel toward the lower pCa. An adenine nucleotide increased the rate of the CICR, but it did not change the range of effective [Ca2+]. 5 mM caffeine greatly enhanced the CICR mechanism, making it approximately 30 times more sensitive to [Ca2+]. However the drug had no Ca-releasing action in the absence of Ca2+. Procaine in millimolar concentrations inhibited the rate of the CICR. These properties are similar to those of the skeletal muscle CICR and ryanodine receptor channels. Rates of the CICR under a physiological ionic milieu were estimated from the results, and a [Ca2+] greater than 1 microM was expected to be necessary for the activation of the Ca release. This Ca sensitivity seems too low for the CICR mechanism to play a primary physiological role in Ca mobilization, unless assisted by other mechanisms.

Metabolic syndrome inhibits store-operated Ca2+ entry and calcium-induced calcium-release mechanism in coronary artery smooth muscle

2020 ◽  
Vol 182 ◽  
pp. 114222
Author(s):  
Belén Climent ◽  
Elvira Santiago ◽  
Ana Sánchez ◽  
Mercedes Muñoz-Picos ◽  
Francisco Pérez–Vizcaíno ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Calcium Release ◽  
Release Mechanism ◽  
Calcium Induced Calcium Release

Chemical modification of calcium release from the sarcoplasmic reticulum of mechanically skinned skeletal bullfrog muscle fibers

1986 ◽  
Vol 64 (10) ◽  
pp. 1267-1271 ◽  
Author(s):  
Takako Aoki ◽  
Toshiharu Oba ◽  
Ken Hotta
Keyword(s):  
Skeletal Muscle ◽  
Amino Acid ◽  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Release Mechanism ◽  
Trinitrobenzenesulfonic Acid ◽  
Amino Acid Side Chains ◽  
Chloramine T ◽  
Tension Curve ◽  
Calcium Induced Calcium Release

Several types of reagents that react with amino acid side chains induced repetitive phasic contracture of skinned skeletal muscle from frogs. The presence of 10 mM procaine or 5 mM magnesium in the medium or disruption of the sarcoplasmic reticulum (SR) eliminated this contracture, indicating that the calcium-induced calcium-release mechanism of SR is involved in the contraction. Dithiothreitol inhibited the contracture induced by chloramine T, N-acetylimidazole, or p-chloromercuriphenylsulfonic acid (pCMPS) but not in the case of carbodiimide, phenylglyoxal, trinitrobenzenesulfonic acid, diethylpyrocarbonate (DEP), or N-chlorosuccinimide (NCS). Therefore, modification of groups other than the sulfhydryl ones seems to induce contractures under such conditions. The amplitude of the caffeine-induced contracture decreased after treatment with pCMPS, DEP, or NCS. NCS shifted the pCa–tension curve toward low pCa in the SR-disrupted fibers. This shift would explain the decrease in caffeine contracture. It is tentatively concluded that pCMPS and DEP release a large amount of calcium from SR.

scholarly journals The Voltage-sensitive Release Mechanism of Excitation Contraction Coupling in Rabbit Cardiac Muscle Is Explained by Calcium-induced Calcium Release

2003 ◽  
Vol 121 (5) ◽  
pp. 353-373 ◽  
Author(s):  
H. Griffiths ◽  
K.T. MacLeod
Keyword(s):  
Calcium Release ◽  
Outward Current ◽  
Disulfonic Acid ◽  
Release Mechanism ◽  
Tonic Component ◽  
Excitation Contraction Coupling ◽  
Inward Current ◽  
Contraction Coupling ◽  
Cell Shortening ◽  
Calcium Induced Calcium Release

The putative voltage-sensitive release mechanism (VSRM) was investigated in rabbit cardiac myocytes at 37°C with high resistance microelectrodes to minimize intracellular dialysis. When the holding potential was adjusted from −40 to −60 mV, the putative VSRM was expected to operate alongside CICR. Under these conditions however, we did not observe a plateau at positive potentials of the cell shortening versus voltage relationship. The threshold for cell shortening changed by −10 mV, but this resulted from a similar change of the threshold for activation of inward current. Cell shortening under conditions where the putative VSRM was expected to operate was blocked in a dose dependent way by nifedipine and CdCl2 and blocked completely by NiCl2. “Tail contractions” persisted in the presence of nifedipine and CdCl2 but were blocked completely by NiCl2. Block of early outward current by 4-aminopyridine and 4-acetoamido-4′-isothiocyanato-stilbene-2,2′-disulfonic acid (SITS) demonstrated persisting inward current during test depolarizations despite the presence of nifedipine and CdCl2. Inward current did not persist in the presence of NiCl2. A tonic component of cell shortening that was prominent during depolarizations to positive potentials under conditions selective for the putative VSRM was sensitive to rapidly applied changes in superfusate [Na+] and to the outward Na+/Ca2+ exchange current blocking drug KB-R7943. This component of cell shortening was thought to be the result of Na+/Ca2+ exchange–mediated excitation contraction coupling. Cell shortening recorded under conditions selective for the putative VSRM was increased by the enhanced state of phosphorylation induced by isoprenaline (1 μM) and by enhancing sarcoplasmic reticulum Ca2+ content by manipulation of the conditioning steps. Under these conditions, cell shortening at positive test depolarizations was converted from tonic to phasic. We conclude that the putative VSRM is explained by CICR with the Ca2+ “trigger” supplied by unblocked L-type Ca2+ channels and Na+/Ca2+ exchange.

scholarly journals Model of calcium-induced calcium release mechanism in cardiac cells

1992 ◽  
Vol 54 (1) ◽  
pp. 95-116 ◽  
Author(s):  
Alan Y. K. Wong ◽  
Alexandre Fabiato ◽  
James B. Bassingthwaighthe
Keyword(s):  
Calcium Release ◽  
Cardiac Cells ◽  
Release Mechanism ◽  
Calcium Induced Calcium Release

Spaceflight regulates ryanodine receptor subtype 1 in portal vein myocytes in the opposite way of hypertension

2012 ◽  
Vol 112 (3) ◽  
pp. 471-480 ◽  
Author(s):  
Fabrice Dabertrand ◽  
Yves Porte ◽  
Nathalie Macrez ◽  
Jean-Luc Morel
Keyword(s):  
Blood Pressure ◽  
Portal Vein ◽  
Ryanodine Receptor ◽  
Calcium Release ◽  
Physiological Adaptation ◽  
Release Mechanism ◽  
Receptor Subtype ◽  
Gravity Level ◽  
Calcium Signals ◽  
Calcium Induced Calcium Release

Gravity has a structural role for living systems. Tissue development, architecture, and organization are modified when the gravity vector is changed. In particular, microgravity induces a redistribution of blood volume and thus pressure in the astronaut body, abolishing an upright blood pressure gradient, inducing orthostatic hypotension. The present study was designed to investigate whether isolated vascular smooth muscle cells are directly sensitive to altered gravitational forces and, second, whether sustained blood pressure changes act on the same molecular target. Exposure to microgravity during 8 days in the International Space Station induced the decrease of ryanodine receptor subtype 1 expression in primary cultured myocytes from rat hepatic portal vein. Identical results were found in portal vein from mice exposed to microgravity during an 8-day shuttle spaceflight. To evaluate the functional consequences of this physiological adaptation, we have compared evoked calcium signals obtained in myocytes from hindlimb unloaded rats, in which the shift of blood pressure mimics the one produced by the microgravity, with those obtained in myocytes from rats injected with antisense oligonucleotide directed against ryanodine receptor subtype 1. In both conditions, calcium signals implicating calcium-induced calcium release were significantly decreased. In contrast, in spontaneous hypertensive rat, an increase in ryanodine receptor subtype 1 expression was observed as well as the calcium-induced calcium release mechanism. Taken together, our results shown that myocytes were directly sensitive to gravity level and that they adapt their calcium signaling pathways to pressure by the regulation of the ryanodine receptor subtype 1 expression.

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