scholarly journals Arginine promotes myogenic differentiation and myotube formation through the elevation of cytoplasmic calcium concentration

2021 ◽  
Author(s):  
Lu Gong ◽  
Xin Zhang ◽  
Kai Qiu ◽  
Linjuan He ◽  
Yubo Wang ◽  
...  
2000 ◽  
Vol 279 (1) ◽  
pp. F92-F101 ◽  
Author(s):  
Michel Bidet ◽  
Guy De Renzis ◽  
Sonia Martial ◽  
Isabelle Rubera ◽  
Michel Tauc ◽  
...  

Experiments were performed to characterize the P2 purinoceptor subtype responsible for cytoplasmic calcium mobilization in cells from the initial part of rabbit distal convoluted tubule (DCT). Free calcium concentration was measured in a DCT cell line (DC1) with the probe fura 2. Both ATP and UTP increased cytosolic Ca2+ concentration ([Ca2+]i; EC50 3 and 6 μM, respectively). The order of potency for nucleotide analogs was ATP = UTP > adenosine 5′- O-[thiotriphosphate] ≫ ADP > UDP, which is consistent with the pharmacology of the P2Y2 receptor subtype. The increased [Ca2+]iresponses to ATP and UTP were strongly inhibited by suramin. Pretreatment of cells with pertussis toxin (PTX) attenuated the action of both nucleotides. Inhibition of phospholipase C with U-73122 totally blocked the [Ca2+]i response to ATP. Thus ATP- and UTP-stimulated [Ca2+]i mobilization in DC1 cells appears to be mediated via the activation of P2Y2 purinoceptors coupled to a G protein mechanism that is partially sensitive to PTX. Calcium flux measurements showed that lanthanum- and nifedipine-sensitive calcium channels are involved in the [Ca2+]i response to ATP.


1993 ◽  
Vol 265 (1) ◽  
pp. H74-H82 ◽  
Author(s):  
P. He ◽  
F. E. Curry

Albumin is required in vascular perfusates to maintain the normal permeability of microvessel walls. The most common mechanism proposed for action of albumin involves binding to the endothelial cell surface to increase the resistance to water and solute flows through hydraulic pathways across the capillary wall. The results of the present experiments do not conform to this simple adsorption model. Ringer perfusion increased the hydraulic conductivity (Lp) of the wall of single perfused frog mesenteric microvessels by 4.0 +/- 0.5-fold. The increase in Lp was associated with an increase of cytoplasmic calcium concentration ([Ca2+]i) from 59 +/- 5 nM when albumin was in the perfusate to a transient peak of 181 +/- 13 nM, 1–2 min after Ringer perfusion. [Ca2+]i then fell back to close to 100 nM. Processes that reduced Ca2+ influx into endothelial cells (removal of extracellular Ca2+, membrane depolarization) reduced Ca2+ influx and attenuated the increase in [Ca2+]i. The same processes abolished the increase in Lp after Ringer perfusion and restored Lp to close to control values during Ringer perfusion. Thus Ca2+ entry into endothelial cells is required to initiate and maintain the increased permeability during Ringer perfusion.


2010 ◽  
Vol 299 (4) ◽  
pp. E517-E532 ◽  
Author(s):  
L. E. Fridlyand ◽  
N. Tamarina ◽  
L. H. Philipson

Oscillatory phenomenon in electrical activity and cytoplasmic calcium concentration in response to glucose are intimately connected to multiple key aspects of pancreatic β-cell physiology. However, there is no single model for oscillatory mechanisms in these cells. We set out to identify possible pacemaker candidates for burst activity and cytoplasmic Ca2+ oscillations in these cells by analyzing published hypotheses, their corresponding mathematical models, and relevant experimental data. We found that although no single pacemaker can account for the variety of oscillatory phenomena in β-cells, at least several separate mechanisms can underlie specific kinds of oscillations. According to our analysis, slowly activating Ca2+-sensitive K+ channels can be responsible for very fast Ca2+ oscillations; changes in the ATP/ADP ratio and in the endoplasmic reticulum calcium concentration can be pacemakers for both fast bursts and cytoplasmic calcium oscillations, and cyclical cytoplasmic Na+ changes may underlie patterning of slow calcium oscillations. However, these mechanisms still lack direct confirmation, and their potential interactions raises new issues. Further studies supported by improved mathematical models are necessary to understand oscillatory phenomena in β-cell physiology.


2006 ◽  
Vol 291 (4) ◽  
pp. F761-F769 ◽  
Author(s):  
János Pittner ◽  
Kristie Rhinehart ◽  
Thomas L. Pallone

Using fura 2-loaded vessels, we tested whether ouabain modulates endothelial cytoplasmic calcium concentration ([Ca2+]CYT) in rat descending vasa recta (DVR). Over a broad range between 10−10 and 10−4 M, ouabain elicited biphasic peak and plateau [Ca2+]CYT elevations. Blockade of voltage-gated Ca2+ entry with nifedipine did not affect the response to ouabain mitigating against a role for myo-endothelial gap junctions. Reduction of extracellular Na+ concentration ([Na+]o) or Na+/Ca2+ exchanger (NCX) inhibition with SEA-0400 (10−6 M) elevated [Ca2+]CYT, supporting a role for NCX in the setting of basal [Ca2+]CYT. SEA-0400 abolished the [Ca2+]CYT response to ouabain implicating NCX as a mediator. The transient peak phase of [Ca2+]CYT elevation that followed either ouabain or reduction of [Na+]o was abolished by 2-aminoethoxydiphenyl borate (5 × 10−5 M). Cation channel blockade with La3+ (10 μM) or SKF-96365 (10 μM) also attenuated the ouabain-induced [Ca2+]CYT response. Ouabain pretreatment increased the [Ca2+]CYT elevation elicited by bradykinin (10−7 M). We conclude that inhibition of ouabain-sensitive Na+-K+-ATPase enhances DVR endothelial Ca2+ store loading and modulates [Ca2+]CYT signaling through mechanisms that involve NCX, Ca2+ release, and cation channel activation.


Planta ◽  
1991 ◽  
Vol 184 (2) ◽  
pp. 166-174 ◽  
Author(s):  
R. Scheuerlein ◽  
K. Schmidt ◽  
M. Poenie ◽  
S. J. Roux

Nature ◽  
1986 ◽  
Vol 321 (6073) ◽  
pp. 888-888 ◽  
Author(s):  
A. B. MacDermott ◽  
M. L. Meyer ◽  
G. L. Westbrook ◽  
S. J. Smith ◽  
J. L. Barker

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