Mitochondrial Ca2+ uptake is important over low [Ca2+]i range in arterial smooth muscle

2002 ◽  
Vol 283 (6) ◽  
pp. H2431-H2439 ◽  
Author(s):  
Tomoko Kamishima ◽  
John M. Quayle
Keyword(s):  
Smooth Muscle ◽  
Decay Time ◽  
Removal Rate ◽  
Arterial Smooth Muscle ◽  
Carbonyl Cyanide ◽  
Before And After ◽  
Intracellular Ca ◽  
Arterial Smooth Muscle Cells ◽  
Time Required ◽  
Loaded Voltage

Mitochondrial Ca2+ uptake is usually thought to occur only when intracellular Ca2+concentration ([Ca2+]i) is high. We investigated whether mitochondrial Ca2+ removal participates in shaping [Ca2+]i signals in arterial smooth muscle over a low [Ca2+]irange. [Ca2+]i was measured using fura 2-loaded, voltage-clamped cells from rat femoral arteries. Both diazoxide and carbonyl cyanide m-chlorophenylhydrazone (CCCP) depolarized the mitochondria. Diazoxide application increased resting [Ca2+]i, suggesting that Ca2+ is sequestered in mitochondria. Over a low [Ca2+]i range, diazoxide and CCCP slowed Ca2+ removal rate, determined after a brief depolarization. When [Ca2+]i was measured during sustained depolarization to −30 mV, CCCP application increased [Ca2+]i. When Ca2+ transients were repeatedly evoked by caffeine applications, CCCP application elevated resting [Ca2+]i. Caffeine-induced Ca2+ transients were compared before and after CCCP application using the half decay time, or time required to reduce increase in [Ca2+]i by 50% ( t ½). CCCP treatment significantly increased t ½. These results suggest that Ca2+ removal to mitochondria in arterial smooth muscle cells may be important at a low [Ca2+]i.

Mobilization of intracellular Ca2+ by endothelin-1 in rat intrapulmonary arterial smooth muscle cells

2000 ◽  
Vol 278 (1) ◽  
pp. L157-L164 ◽  
Author(s):  
Larissa A. Shimoda ◽  
J. T. Sylvester ◽  
James S. K. Sham
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Voltage Gated ◽  
Endothelin 1 ◽  
Intracellular Release ◽  
Intracellular Ca ◽  
Pulmonary Arterial ◽  
Arterial Smooth Muscle Cells

Endothelin-1 (ET-1) increases intracellular Ca2+ concentration ([Ca2+]i) in pulmonary arterial smooth muscle cells (PASMCs); however, the mechanisms for Ca2+ mobilization are not clear. We determined the contributions of extracellular influx and intracellular release to the ET-1-induced Ca2+ response using Indo 1 fluorescence and electrophysiological techniques. Application of ET-1 (10−10 to 10−8 M) to transiently (24–48 h) cultured rat PASMCs caused concentration-dependent increases in [Ca2+]i. At 10−8 M, ET-1 caused a large, transient increase in [Ca2+]i (>1 μM) followed by a sustained elevation in [Ca2+]i(<200 nM). The ET-1-induced increase in [Ca2+]i was attenuated (<80%) by extracellular Ca2+ removal; by verapamil, a voltage-gated Ca2+-channel antagonist; and by ryanodine, an inhibitor of Ca2+ release from caffeine-sensitive stores. Depleting intracellular stores with thapsigargin abolished the peak in [Ca2+]i, but the sustained phase was unaffected. Simultaneously measuring membrane potential and [Ca2+]i indicated that depolarization preceded the rise in [Ca2+]i. These results suggest that ET-1 initiates depolarization in PASMCs, leading to Ca2+influx through voltage-gated Ca2+ channels and Ca2+ release from ryanodine- and inositol 1,4,5-trisphosphate-sensitive stores.

Phosphatidylinositol 3,5-bisphosphate increases intracellular free Ca2+ in arterial smooth muscle cells and elicits vasocontraction

2011 ◽  
Vol 300 (6) ◽  
pp. H2016-H2026 ◽  
Author(s):  
Neerupma Silswal ◽  
Nikhil K. Parelkar ◽  
Michael J. Wacker ◽  
Marco Brotto ◽  
Jon Andresen
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Ryanodine Receptors ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Arterial Smooth Muscle Cells

Phosphoinositide (3,5)-bisphosphate [PI(3,5)P2] is a newly identified phosphoinositide that modulates intracellular Ca2+ by activating ryanodine receptors (RyRs). Since the contractile state of arterial smooth muscle depends on the concentration of intracellular Ca2+, we hypothesized that by mobilizing sarcoplasmic reticulum (SR) Ca2+ stores PI(3,5)P2 would increase intracellular Ca2+ in arterial smooth muscle cells and cause vasocontraction. Using immunohistochemistry, we found that PI(3,5)P2 was present in the mouse aorta and that exogenously applied PI(3,5)P2 readily entered aortic smooth muscle cells. In isolated aortic smooth muscle cells, exogenous PI(3,5)P2 elevated intracellular Ca2+, and it also contracted aortic rings. Both the rise in intracellular Ca2+ and the contraction caused by PI(3,5)P2 were prevented by antagonizing RyRs, while the majority of the PI(3,5)P2 response was intact after blockade of inositol (1,4,5)-trisphosphate receptors. Depletion of SR Ca2+ stores with thapsigargin or caffeine and/or ryanodine blunted the Ca2+ response and greatly attenuated the contraction elicited by PI(3,5)P2. The removal of extracellular Ca2+ or addition of verapamil to inhibit voltage-dependent Ca2+ channels reduced but did not eliminate the Ca2+ or contractile responses to PI(3,5)P2. We also found that PI(3,5)P2 depolarized aortic smooth muscle cells and that LaCl3 inhibited those aspects of the PI(3,5)P2 response attributable to extracellular Ca2+. Thus, full and sustained aortic contractions to PI(3,5)P2 required the release of SR Ca2+, probably via the activation of RyR, and also extracellular Ca2+ entry via voltage-dependent Ca2+ channels.

Nitric oxide inhibits Ca2+ mobilization through cADP-ribose signaling in coronary arterial smooth muscle cells

2000 ◽  
Vol 279 (3) ◽  
pp. H873-H881 ◽  
Author(s):  
Jiang-Zhou Yu ◽  
David X. Zhang ◽  
Ai-Ping Zou ◽  
William B. Campbell ◽  
Pin-Lan Li
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Inhibitory Effect ◽  
Cyclase Activity ◽  
Arterial Smooth Muscle ◽  
Adp Ribosyl Cyclase ◽  
Intracellular Ca ◽  
Arterial Smooth Muscle Cells

The present study was designed to determine whether the cADP-ribose-mediated Ca2+ signaling is involved in the inhibitory effect of nitric oxide (NO) on intracellular Ca2+ mobilization. With the use of fluorescent microscopic spectrometry, cADP-ribose-induced Ca2+ release from sarcoplasmic reticulum (SR) of bovine coronary arterial smooth muscle cells (CASMCs) was determined. In the α-toxin-permeabilized primary cultures of CASMCs, cADP-ribose (5 μM) produced a rapid Ca2+ release, which was completely blocked by pretreatment of cells with the cADP-ribose antagonist 8-bromo-cADP-ribose (8-Br-cADPR). In intact fura 2-loaded CASMCs, 80 mM KCl was added to depolarize the cells and increase intracellular Ca2+ concentration ([Ca2+]i). Sodium nitroprusside (SNP), an NO donor, produced a concentration-dependent inhibition of the KCl-induced increase in [Ca2+]i, but it had no effect on the U-46619-induced increase in [Ca2+]i. In the presence of 8-Br-cADPR (100 μM) and ryanodine (10 μM), the inhibitory effect of SNP was markedly attenuated. HPLC analyses showed that CASMCs expressed the ADP-ribosyl cyclase activity, and SNP (1–100 μM) significantly reduced the ADP-ribosyl cyclase activity in a concentration-dependent manner. The effect of SNP was completely blocked by addition of 10 μM oxygenated hemoglobin. We conclude that ADP-ribosyl cyclase is present in CASMCs, and NO may decrease [Ca2+]i by inhibition of cADP-ribose-induced Ca2+ mobilization.

Hydrogen peroxide-induced Ca2+ mobilization in pulmonary arterial smooth muscle cells

2007 ◽  
Vol 292 (6) ◽  
pp. L1598-L1608 ◽  
Author(s):  
Mo-Jun Lin ◽  
Xiao-Ru Yang ◽  
Yuan-Ning Cao ◽  
James S. K. Sham
Keyword(s):  
Hydrogen Peroxide ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Channel Blockers ◽  
Arterial Smooth Muscle ◽  
Intracellular Ca ◽  
Pulmonary Arterial ◽  
Arterial Smooth Muscle Cells ◽  
Pulmonary Arterial Smooth Muscle

Reactive oxygen species (ROS) generated from NADPH oxidases and mitochondria have been implicated as key messengers for pulmonary vasoconstriction and vascular remodeling induced by agonists and hypoxia. Since Ca2+ mobilization is essential for vasoconstriction and cell proliferation, we sought to characterize the Ca2+ response and to delineate the Ca2+ pathways activated by hydrogen peroxide (H2O2) in rat intralobar pulmonary arterial smooth muscle cells (PASMCs). Exogenous application of 10 μM to 1 mM H2O2 elicited concentration-dependent increase in intracellular Ca2+ concentration in PASMCs, with an initial rise followed by a plateau or slow secondary increase. The initial phase was related to intracellular release. It was attenuated by the inositol trisphosphate (IP3) receptor antagonist 2-aminoethyl diphenylborate, ryanodine, or thapsigargin, but was unaffected by the removal of Ca2+ in external solution. The secondary phase was dependent on extracellular Ca2+ influx. It was unaffected by the voltage-gated Ca2+ channel blocker nifedipine or the nonselective cation channel blockers SKF-96365 and La3+, but inhibited concentration dependently by millimolar Ni2+, and potentiated by the Na+/Ca2+ exchange inhibitor KB-R 7943. H2O2 did not alter the rate of Mn2+ quenching of fura 2, suggesting store- and receptor-operated Ca2+ channels were not involved. By contrast, H2O2 elicited a sustained inward current carried by Na+ at −70 mV, and the current was inhibited by Ni2+. These results suggest that H2O2 mobilizes intracellular Ca2+ through multiple pathways, including the IP3- and ryanodine receptor-gated Ca2+ stores, and Ni2+-sensitive cation channels. Activation of these Ca2+ pathways may play important roles in ROS signaling in PASMCs.

Heterogeneity of calcium stores and elementary release events in canine pulmonary arterial smooth muscle cells

2001 ◽  
Vol 280 (1) ◽  
pp. C22-C33 ◽  
Author(s):  
Robert Janiak ◽  
Sean M. Wilson ◽  
Stephen Montague ◽  
Joseph R. Hume
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Laser Scanning Microscopy ◽  
Calcium Stores ◽  
Ang Ii ◽  
Arterial Smooth Muscle ◽  
Intracellular Ca ◽  
Pulmonary Arterial ◽  
Arterial Smooth Muscle Cells

To examine the nature of inositol 1,4,5-trisphosphate (IP3)-sensitive and ryanodine (Ryn)-sensitive Ca2+ stores in isolated canine pulmonary arterial smooth cells (PASMC), agonist-induced changes in global intracellular Ca2+ concentration ([Ca2+]i) were measured using fura 2-AM fluorescence. Properties of elementary local Ca2+release events were characterized using fluo 3-AM or fluo 4-AM, in combination with confocal laser scanning microscopy. In PASMC, depletion of sarcoplasmic reticulum Ca2+ stores with Ryn (300 μM) and caffeine (Caf; 10 mM) eliminated subsequent Caf-induced intracellular Ca2+ transients but had little or no effect on the initial IP3-mediated intracellular Ca2+transient induced by ANG II (1 μM). Cyclopiazonic acid (CPA; 10 μM) abolished IP3-induced intracellular Ca2+ transients but failed to attenuate the initial Caf-induced intracellular Ca2+ transient. These results suggest that in canine PASMC, IP3-, and Ryn-sensitive Ca2+ stores are organized into spatially distinct compartments while similar experiments in canine renal arterial smooth muscle cells (RASMC) reveal that these Ca2+ stores are spatially conjoined. In PASMC, spontaneous local intracellular Ca2+ transients sensitive to modulation by Caf and Ryn were detected, exhibiting spatial-temporal characteristics similar to those previously described for “Ca2+ sparks” in cardiac and other types of smooth muscle cells. After depletion of Ryn-sensitive Ca2+ stores, ANG II (8 nM) induced slow, sustained [Ca2+]i increases originating at sites near the cell surface, which were abolished by depleting IP3stores. Discrete quantal-like events expected due to the coordinated opening of IP3 receptor clusters (“Ca2+puffs”) were not observed. These data provide new information regarding the functional properties and organization of intracellular Ca2+ stores and elementary Ca2+ release events in isolated PASMC.

scholarly journals Effects of vasopressin on ATP-sensitive and Ca2+-activated K+ channels of coronary arterial smooth muscle cells

1992 ◽  
Vol 58 ◽  
pp. 339
Author(s):  
Tetsuzo Wakatsuki ◽  
Yutaka Nakaya ◽  
Yukiko Miyoshi ◽  
Zeng Xiao-Rong ◽  
Masahiro Nomura ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
K Channels ◽  
Arterial Smooth Muscle Cells
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