scholarly journals Cytosolic calcium and membrane potential in articular chondrocytes during parabolic flight

2022 ◽  
Author(s):  
Simon L. Wuest ◽  
Geraldine Cerretti ◽  
Jennifer Louise Wadsworth ◽  
Cindy Follonier ◽  
Karin F. Rattenbacher-Kiser ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Articular Chondrocytes ◽  
Parabolic Flight ◽  
Cytosolic Calcium

scholarly journals Injection of inositol trisphosphorothioate into Limulus ventral photoreceptors causes oscillations of free cytosolic calcium.

1991 ◽  
Vol 97 (6) ◽  
pp. 1165-1186 ◽  
Author(s):  
R Payne ◽  
B V Potter
Keyword(s):  
Membrane Potential ◽  
Calcium Release ◽  
Feedback Inhibition ◽  
Initial Response ◽  
Periodic Variation ◽  
Cytosolic Calcium ◽  
Ion Concentration ◽  
Free Calcium ◽  
Calcium Stores ◽  
Calcium Ion Concentration

Limulus ventral photoreceptors contain calcium stores sensitive to release by D-myo-inositol 1,4,5 trisphosphate (InsP3) and a calcium-activated conductance that depolarizes the cell. Mechanisms that terminate the response to InsP3 were investigated using nonmetabolizable DL-myo-inositol 1,4,5 trisphosphorothioate (InsPS3). An injection of 1 mM InsPS3 into a photoreceptor's light-sensitive lobe caused an initial elevation of cytosolic free calcium ion concentration (Cai) and a depolarization lasting only 1-2 s. A period of densensitization followed, during which injections of InsPS3 were ineffective. As sensitivity recovered, oscillations of membrane potential began, continuing for many minutes with a frequency of 0.07-0.3 Hz. The activity of InsPS3 probably results from the D-stereoisomer, since L-InsP3 was much less effective than InsP3. Injections of 1 mM InsP3 caused an initial depolarization and a period of densensitization similar to that caused by 1 mM InsPS3, but no sustained oscillations of membrane potential. The initial response to InsPS3 or InsP3 may therefore be terminated by densensitization, rather than by metabolism. Metabolism of InsP3 may prevent oscillations of membrane potential after sensitivity has recovered. The InsPS3-induced oscillations of membrane potential accompanied oscillations of Cai and were abolished by injection of ethyleneglycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid. Removal of extracellular calcium reduced the frequency of oscillation but not its amplitude. Under voltage clamp, oscillations of inward current were observed. These results indicate that periodic bursts of calcium release underly the oscillations of membrane potential. After each burst, the sensitivity of the cell to injected InsP3 was greatly reduced, recovering during the interburst interval. The oscillations may, therefore, result in part from a periodic variation in sensitivity to a constant concentration of InsPS3. Prior injection of calcium inhibited depolarization by InsPS3, suggesting that feedback inhibition of InsPS3-induced calcium release by elevated Cai may mediate desensitization between bursts and after injections of InsPS3.

scholarly journals Modelling the Membrane Potential Dependence on Non-Specific Cation Channels in Canine Articular Chondrocytes

2010 ◽  
Vol 98 (3) ◽  
pp. 340a
Author(s):  
Rebecca Lewis ◽  
Gregor Purves ◽  
Julia Crossley ◽  
Richard Barrett-Jolley
Keyword(s):  
Membrane Potential ◽  
Articular Chondrocytes ◽  
Cation Channels ◽  
Potential Dependence

Opposite effects of redox status on membrane potential, cytosolic calcium, and tone in pulmonary arteries and ductus arteriosus

2004 ◽  
Vol 286 (1) ◽  
pp. L15-L22 ◽  
Author(s):  
Andrea Olschewski ◽  
Zhigang Hong ◽  
Douglas A. Peterson ◽  
Daniel P. Nelson ◽  
Valerie A. Porter ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Oxygen Tension ◽  
Potassium Current ◽  
Ductus Arteriosus ◽  
Pulmonary Arteries ◽  
Cytosolic Calcium ◽  
Redox Status ◽  
Hypoxic Conditions ◽  
Potent Vasodilator ◽  
Oxygen Signaling

At birth, associated with the rise in oxygen tension, the pulmonary arteries (PA) dilate and the ductus arteriosus (DA) constricts. Both PA and DA constrict with vasoconstrictors and dilate with vasodilators. They respond in a contrary manner only to changes in oxygen tension. We hypothesized that the effects of changes in oxygen are mediated by changes in redox status. Consequently, we tested whether a reducing agent, DTT, and an oxidizing agent, dithionitrobenzoic acid (DTNB), would have opposite effects on a major oxygen signaling pathway in the PA and DA smooth muscle cells (SMCs), the sequence of change in potassium current ( IK), membrane potential ( Em), cytosolic calcium, and vessel tone. Under normoxic conditions, DTT constricted adult and fetal resistance PA rings, whereas in DA rings DTT acted as a potent vasodilator. In normoxia, voltage-clamp measurements showed inhibition of IK by DTT in PASMCs and, in contrast, activation in DASMCs. Consequently, DTT depolarized fetal and adult PASMCs and hyperpolarized DASMCs. [Ca2+]i was increased by DTT in fetal and adult PASMCs and decreased in DASMCs. Under hypoxic conditions, DTNB constricted DA rings and caused vasodilatation in fetal PA rings. DTNB inhibited IK and depolarized the cell membrane in DASMCs. In contrast, activation of IK and hyperpolarization was seen in PASMCs. Thus the same redox signal can elicit opposite effects on IK, Em, cytosolic calcium, and vascular tone in resistance PA and the DA. These observations support the concept that redox changes could signal the opposite effects of oxygen in the PA and DA.

scholarly journals A voltage-dependent K+current contributes to membrane potential of acutely isolated canine articular chondrocytes

2004 ◽  
Vol 557 (1) ◽  
pp. 93-104 ◽  
Author(s):  
Jim R. Wilson ◽  
Neil A. Duncan ◽  
Wayne R. Giles ◽  
Robert B. Clark
Keyword(s):  
Membrane Potential ◽  
Articular Chondrocytes ◽  
Voltage Dependent ◽  
K Current

Effect of membrane potential on cytosolic calcium of bovine aortic endothelial cells

1989 ◽  
Vol 257 (3) ◽  
pp. H778-H784 ◽  
Author(s):  
W. P. Schilling
Keyword(s):  
Endothelial Cells ◽  
Membrane Potential ◽  
Cytosolic Calcium ◽  
Membrane Depolarization ◽  
K Channel ◽  
Membrane Hyperpolarization ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
K Concentration ◽  
Aortic Endothelial

The effect of bradykinin on membrane potential of cultured bovine aortic endothelial cells (BAECs) was estimated by measuring the uptake of the lipophilic cation, tetra[3H]phenylphosphonium ([3H]TPP+). Uptake of [3H]TPP+ was found to be 1) a function of extracellular K+ concentration, 2) sensitive to valinomycin, and 3) decreased by the K+ channel inhibitor, Ba2+, suggesting that the uptake of [3H]TPP+ responds to changes in membrane potential of the BAEC. Bradykinin (50 nM) produced an increase in [3H]TPP+ uptake in low K+ buffer consistent with a bradykinin-induced membrane hyperpolarization. The effect of membrane depolarization with high K+ buffer on the bradykinin-stimulated changes in cytosolic Ca2+ was determined using the fluorescent Ca2+ indicator, fura-2. The results of these experiments demonstrated that both basal cytosolic Ca2+ and bradykinin-stimulated release of Ca2+ from internal stores were not affected by membrane depolarization. However, bradykinin-stimulated influx of Ca2+ from the extracellular space decreased with membrane depolarization in a manner consistent with the movement of Ca2+ through a channel.

Cytosolic Calcium Oscillations in Smooth Muscle Cells

Physiology ◽  
2000 ◽  
Vol 15 (1) ◽  
pp. 50-55 ◽  
Author(s):  
Jean-Pierre Savineau ◽  
Roger Marthan
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Smooth Muscle Cells ◽  
Inositol Trisphosphate ◽  
Muscle Cells ◽  
Cytosolic Calcium ◽  
Calcium Oscillations ◽  
Membrane Receptors ◽  
Cell Membrane Potential

In a variety of smooth muscle cells, agonists activating membrane receptors induce oscillations in the cytoplasmic Ca2+ concentration via an inositol trisphosphate-activated mechanism. Ca2+ oscillations participate in the control of cell membrane potential and the tone of smooth muscle. There is evidence that alterations in Ca2+ oscillations modulate smooth muscle responsiveness.

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