Focal sarcoplasmic reticulum calcium stores and diffuse inositol 1,4,5-trisphosphate and ryanodine receptors in human myometrium

Cell Calcium ◽  
1999 ◽  
Vol 26 (1-2) ◽  
pp. 69-75 ◽  
Author(s):  
R.C. Young ◽  
S.P. Mathur
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ryanodine Receptors ◽  
Human Myometrium ◽  
Calcium Stores ◽  
Inositol 1,4,5 Trisphosphate ◽  
Sarcoplasmic Reticulum Calcium

Sarcoplasmic Reticulum Calcium Release Channels in Ventricles of Older Adult Hamsters

2006 ◽  
Vol 25 (1) ◽  
pp. 107-113 ◽  
Author(s):  
Peter A. Nicholl ◽  
Susan E. Howlett
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Older Adult ◽  
Binding Sites ◽  
Calcium Release ◽  
Ryanodine Receptors ◽  
Calcium Release Channels ◽  
Site Density ◽  
Age Related ◽  
Sarcoplasmic Reticulum Calcium ◽  
Age Related Changes

ABSTRACTWhether the density of sarcoplasmic reticulum (SR) calcium release channels / ryanodine receptors in the heart declines with age is not clear. We investigated age-related changes in the density of «3H»-ryanodine receptors in crude ventricular homogenates, which contained all ligand binding sites in heart and in isolated junctional SR membranes. Experiments utilized young (120 days) and older adult (300 days) hamsters. «3H»-ryanodine binding site density did not change with age in crude homogenate preparations, although total heart protein concentration increased significantly with age. In contrast, the density of «3H»-ryanodine binding sites decreased markedly in heavy SR membranes purified from older hearts. These results show that demonstration of age-related changes in cardiac ryanodine receptor density depends upon the preparation used. Furthermore, the increase in total ventricular protein with age suggests that normalization of data by membrane protein should be used with caution in studies of aging heart.

Nitric oxide inhibits calcium release from sarcoplasmic reticulum of porcine tracheal smooth muscle cells

1997 ◽  
Vol 272 (1) ◽  
pp. L1-L7 ◽  
Author(s):  
M. S. Kannan ◽  
Y. S. Prakash ◽  
D. E. Johnson ◽  
G. C. Sieck
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Ryanodine Receptors ◽  
Tracheal Smooth Muscle ◽  
Nitric Oxide Donor ◽  
Ip3 Receptors ◽  
Video Fluorescence Microscopy ◽  
Inositol 1,4,5 Trisphosphate

In the present study, effects of the nitric oxide donor, S-nitroso-N-acetylpenicillamine (SNAP), on sarcoplasmic reticulum (SR) Ca2+ release were examined in freshly dissociated porcine tracheal smooth muscle (TSM) cells. Fura 2-loaded TSM cells were imaged using video fluorescence microscopy. SR Ca2+ release was induced by acetylcholine (ACh), which acts principally through inositol 1,4,5-trisphosphate (IP3) receptors, and by caffeine, which acts principally through ryanodine receptors (RyR). SNAP inhibited ACh-induced SR Ca2+ release at both 0 and 2.5 mM extracellular Ca2+. Degraded SNAP had no effect on ACh-induced SR Ca2+ release. SNAP also inhibited caffeine-induced SR Ca2+ release. ACh-induced Ca2+ influx was not affected by SNAP when SR reloading was blocked by thapsigargin. SNAP also did not affect SR Ca2+ reuptake. The membrane-permeant analogue of guanosine 3',5'-cyclic monophosphate (cGMP), 8-bromo-cGMP, mimicked the effects of SNAP. These results suggest that, in porcine TSM cells, SNAP reduces the intracellular Ca2+ response to ACh and caffeine by inhibiting SR Ca2+ release through both IP3 and RyR, but not by inhibiting influx or repletion of the SR Ca2+ stores. These effects are likely mediated via cGMP-dependent mechanisms.

Intracellular Cl− fluxes play a novel role in Ca2+ handling in airway smooth muscle

2006 ◽  
Vol 290 (6) ◽  
pp. L1146-L1153 ◽  
Author(s):  
Simon Hirota ◽  
Nancy Trimble ◽  
Evi Pertens ◽  
Luke J. Janssen
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Benzoic Acid ◽  
Airway Smooth Muscle ◽  
Channel Blocker ◽  
Negative Charge ◽  
Ryanodine Receptors ◽  
Inositol 1,4,5 Trisphosphate ◽  
Intracellular Ca ◽  
Uptake And Release

Intracellular Ca2+ is actively sequestered into the sarcoplasmic reticulum (SR), whereas the release of Ca2+ from the SR can be triggered by activation of the inositol 1,4,5-trisphosphate and ryanodine receptors. Uptake and release of Ca2+ across the SR membrane are electrogenic processes; accumulation of positive or negative charge across the SR membrane could electrostatically hinder the movement of Ca2+ into or out of the SR, respectively. We hypothesized that the movement of intracellular Cl− (Cl[Formula: see text]) across the SR membrane neutralizes the accumulation of charge that accompanies uptake and release of Ca2+. Thus inhibition of SR Cl− fluxes will reduce Ca2+ sequestration and agonist-induced release. The Cl− channel blocker 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB; 10−4 M), previously shown to inhibit SR Cl− channels, significantly reduced the magnitude of successive acetylcholine-induced contractions of airway smooth muscle (ASM), suggesting a “run down” of sequestered Ca2+ within the SR. Niflumic acid (10−4 M), a structurally different Cl− channel blocker, had no such effect. Furthermore, NPPB significantly reduced caffeine-induced contraction and increases in intracellular Ca2+ concentration ([Ca2+]i). Depletion of Cl[Formula: see text], accomplished by bathing ASM strips in Cl−-free buffer, significantly reduced the magnitude of successive acetylcholine-induced contractions. In addition, Cl− depletion significantly reduced caffeine-induced increases in [Ca2+]i. Together these data suggest a novel role for Cl[Formula: see text] fluxes in Ca2+ handling in smooth muscle. Because the release of sequestered Ca2+ is the predominate source of Ca2+ for contraction of ASM, targeting Cl[Formula: see text] fluxes may prove useful in the control of ASM hyperresponsiveness associated with asthma.

scholarly journals Identification of Functionally Segregated Sarcoplasmic Reticulum Calcium Stores in Pulmonary Arterial Smooth Muscle

2010 ◽  
Vol 285 (18) ◽  
pp. 13542-13549 ◽  
Author(s):  
Jill H. Clark ◽  
Nicholas P. Kinnear ◽  
Svetlana Kalujnaia ◽  
Gordon Cramb ◽  
Sidney Fleischer ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Calcium Stores ◽  
Arterial Smooth Muscle ◽  
Pulmonary Arterial ◽  
Pulmonary Arterial Smooth Muscle ◽  
Sarcoplasmic Reticulum Calcium

Store-operated Ca2+ entry in porcine airway smooth muscle

2004 ◽  
Vol 286 (5) ◽  
pp. L909-L917 ◽  
Author(s):  
Binnaz Ay ◽  
Y. S. Prakash ◽  
Christina M. Pabelick ◽  
Gary C. Sieck
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Airway Smooth Muscle ◽  
Ryanodine Receptors ◽  
Cyclopiazonic Acid ◽  
Inositol 1,4,5 Trisphosphate ◽  
Presence And Absence ◽  
Induced Changes ◽  
Subsequent Introduction

Ca2+ influx triggered by depletion of sarcoplasmic reticulum (SR) Ca2+ stores [mediated via store-operated Ca2+ channels (SOCC)] was characterized in enzymatically dissociated porcine airway smooth muscle (ASM) cells. When SR Ca2+ was depleted by either 5 μM cyclopiazonic acid or 5 mM caffeine in the absence of extracellular Ca2+, subsequent introduction of extracellular Ca2+ further elevated [Ca2+]i. SOCC was insensitive to 1 μM nifedipine- or KCl-induced changes in membrane potential. However, preexposure of cells to 100 nM–1 mM La3+ or Ni2+ inhibited SOCC. Exposure to ACh increased Ca2+ influx both in the presence and absence of a depleted SR. Inhibition of inositol 1,4,5-trisphosphate (IP)-induced SR Ca2+ release by 20 μM xestospongin D inhibited SOCC, whereas ACh-induced IP3 production by 5 μM U-73122 had no effect. Inhibition of Ca2+ release through ryanodine receptors (RyR) by 100 μM ryanodine also prevented Ca2+ influx via SOCC. Qualitatively similar characteristics of SOCC-mediated Ca2+ influx were observed with cyclopiazonic acid- vs. caffeine-induced SR Ca2+ depletion. These data demonstrate that a Ni2+/La3+-sensitive Ca2+ influx via SOCC in porcine ASM cells involves SR Ca2+ release through both IP3 and RyR channels. Additional regulation of Ca2+ influx by agonist may be related to a receptor-operated, noncapacitative mechanism.

Cyclic ADP-ribose stimulates sarcoplasmic reticulum calcium release in porcine coronary artery smooth muscle

1996 ◽  
Vol 270 (2) ◽  
pp. H801-H806 ◽  
Author(s):  
M. S. Kannan ◽  
A. M. Fenton ◽  
Y. S. Prakash ◽  
G. C. Sieck
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Direct Evidence ◽  
Ryanodine Receptors ◽  
Porcine Coronary Artery ◽  
Inositol 1 ◽  
Cyclic Adp Ribose ◽  
Sarcoplasmic Reticulum Calcium

Cyclic ADP-ribose (cADPR) was shown to induce calcium release from the endoplasmic reticulum via ryanodine-sensitive pathways. In smooth muscle, two pathways for calcium release from the sarcoplasmic reticulum (SR) have been previously demonstrated: D-myo-inositol 1, 4, 5-trisphosphate-gated and ryanodine-gated. However, evidence for cADPR as a regulator for SR Ca2+ release in smooth muscle is lacking. We used permeabilized porcine coronary artery smooth muscle cells to directly examine the stimulation of SR Ca2+ release by cADPR. The results provide direct evidence that cADPR stimulates SR Ca2+ release and that this response is not inhibited by heparin, by depletion of the caffeine-sensitive Ca2+ pool, or by blockade or ryanodine receptors. These results indicate a novel mechanism for Ca2+ release from the SR of vascular smooth muscle.

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