Spontaneous oscillations in cytoplasmic calcium concentration in vascular smooth muscle

1989 ◽  
Vol 256 (5) ◽  
pp. C951-C957 ◽  
Author(s):  
P. L. Weissberg ◽  
P. J. Little ◽  
A. Bobik
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Calcium Channel ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Release ◽  
Extracellular Calcium ◽  
Fluorescence Measurement ◽  
Cytoplasmic Calcium ◽  
Spontaneous Oscillations

Fluorescence measurement of fura-2 and quin2 signals from confluent primary cultures of serum-deprived rat aortic smooth muscle cells have revealed spontaneous oscillations in intracellular calcium concentration ([Ca2+]i). The transients consist of a rapid increase in [Ca2+]i that averages 60 nM and lasts approximately 30 s. They are caused by intracellular calcium release and an influx of extracellular calcium. Exposure of cells to the calcium-channel antagonists verapamil and diltiazem or incubation in nominally calcium-free medium reduced both the duration and amplitude of the transients; in contrast, the calcium-channel agonist (-)BAY K 8644 increased their duration. The transients were abolished by caffeine and 8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate, agents that interfere with calcium release from the sarcoplasmic reticulum. These findings demonstrate that the sarcoplasmic reticulum is a primary source for the spontaneous oscillations in cytoplasmic calcium and is closely associated with the influx of extracellular calcium. Although the function of these transients is unclear, they may be involved in the spontaneous contractions observed in some vessels and in the regulation of vascular resistance.

scholarly journals Testosterone inhibits the prostaglandin F2alpha-mediated increase in intracellular calcium in A7r5 aortic smooth muscle cells: evidence of an antagonistic action upon store-operated calcium channels

2003 ◽  
Vol 178 (3) ◽  
pp. 381-393 ◽  
Author(s):  
RD Jones ◽  
LN Ruban ◽  
IE Morton ◽  
SA Roberts ◽  
KM English ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Calcium Channels ◽  
Smooth Muscle Cells ◽  
Calcium Channel ◽  
Intracellular Calcium ◽  
Muscle Cells ◽  
Extracellular Calcium ◽  
Testosterone Replacement Therapy ◽  
Antagonistic Action ◽  
Prostaglandin F

Testosterone-induced vasodilatation is proposed to contribute to the beneficial effects associated with testosterone replacement therapy in men with cardiovascular disease, and is postulated to occur via either direct calcium channel blockade, or through potassium channel activation via increased production of cyclic nucleotides. We utilised flow cytometry to investigate whether testosterone inhibits the increase in cellular fluorescence induced by prostaglandin F(2alpha) in A7r5 smooth muscle cells loaded with the calcium fluorescent probe indo-1-AM, and to study the cellular mechanisms involved. Two-minute incubation with testosterone (1 microM) significantly inhibited the change in cellular fluorescence in response to prostaglandin F(2alpha) (10 microM) (3.6+/-0.6 vs 7.6+/-1.0 arbitrary units, P=0.001). The change in cellular fluorescence in response to prostaglandin F(2alpha) (10 microM) was also significantly attenuated in the absence of extracellular calcium (3.6+/-0.3 vs 15.6+/-0.7 arbitrary units, P=0.0000002), and by a 2-min incubation with the store-operated calcium channel blocker SK&F 96365 (50 microM) (4.7+/-0.8 vs 8.1+/-0.4 arbitrary units, P=0.003). The response was insensitive to similar incubation with the voltage-operated calcium channel blockers verapamil (10 microM) (12.6+/-1.2 vs 11.9+/-0.2 arbitrary units, P=0.7) or nifedipine (10 microM) (13.9+/-1.3 vs 13.3+/-0.5 arbitrary units, P=0.7). Forskolin (1 microM) and sodium nitroprusside (100 microM) significantly increased the cellular concentration of cyclic adenosine monophosphate and cyclic guanosine monophosphate respectively, but testosterone (100 nM-100 microM) had no effect. These data indicate that the increase in intracellular calcium in response to prostaglandin F(2alpha) occurs primarily via extracellular calcium entry through store-operated calcium channels. Testosterone inhibits the response, suggesting an antagonistic action upon these channels.

scholarly journals Genetic ablation of calcium-independent phospholipase A2β causes hypercontractility and markedly attenuates endothelium-dependent relaxation to acetylcholine

2010 ◽  
Vol 298 (6) ◽  
pp. H2208-H2220 ◽  
Author(s):  
Hans H. Dietrich ◽  
Dana R. Abendschein ◽  
Sung Ho Moon ◽  
Neema Nayeb-Hashemi ◽  
David J. Mancuso ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Calcium Influx ◽  
Extracellular Calcium ◽  
Genetic Ablation ◽  
Vasomotor Function ◽  
Intracellular Calcium Release

Activation of phospholipases leads to the release of arachidonic acid and lysophospholipids that play prominent roles in regulating vasomotor tone. To identify the role of calcium-independent phospholipase A2β (iPLA2β) in vasomotor function, we measured vascular responses to phenylephrine (PE) and ACh in mesenteric arterioles from wild-type (WT; iPLA2β+/+) mice and those lacking the β-isoform (iPLA2β−/−) both ex vivo and in vivo. Vessels isolated from iPLA2β−/− mice demonstrated increased constriction to PE, despite lower basal smooth muscle calcium levels, and decreased vasodilation to ACh compared with iPLA2β+/+ mice. PE constriction resulted in initial intracellular calcium release with subsequent steady-state constriction that depended on extracellular calcium influx. Endothelial denudation had no effect on vessel tone or PE-induced constriction although the dilation to ACh was significantly reduced in iPLA2β+/+ vessels. In contrast, vessels from iPLA2β−/− constricted by 54% after denudation, indicating smooth muscle hypercontractility. In vivo, blood pressure, resting vessel diameter, and constriction of mesenteric vessels to PE were not different in iPLA2β−/− vessels compared with WT mouse vessels. However, relaxation after ACh administration in situ was attenuated, indicating an endothelial inability to induce dilation in response to ACh. In cultured endothelial cells, inhibition of iPLA2β with ( S)-(E)-6-(bromomethylene)tetrahydro-3-(1-naphthalenyl)-2 H-pyran-2-one (BEL) decreased endothelial nitric oxide synthase phosphorylation and reduced endothelial agonist-induced intracellular calcium release as well as extracellular calcium influx. We conclude that iPLA2β is an important mediator of vascular relaxation and intracellular calcium homeostasis in both smooth muscle and endothelial cells and that ablation of iPLA2β causes agonist-induced smooth muscle hypercontractility and reduced agonist-induced endothelial dilation.

scholarly journals Orientia tsutsugamushi Inhibits Apoptosis of Macrophages by Retarding Intracellular Calcium Release

2002 ◽  
Vol 70 (8) ◽  
pp. 4692-4696 ◽  
Author(s):  
Mee-Kyung Kim ◽  
Seung-Yong Seong ◽  
Ju-Young Seoh ◽  
Tae-Hee Han ◽  
Hyeon-Je Song ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Release ◽  
Cytosolic Calcium ◽  
Orientia Tsutsugamushi ◽  
Cytosolic Calcium Concentration ◽  
Infected Cells ◽  
Intracellular Calcium Release ◽  
Calcium Redistribution ◽  
In Cells

ABSTRACT Orientia tsutsugamushi shows both pro- and antiapoptotic activities in infected vertebrate cells. Apoptosis of THP-1 cells induced by beauvericin was inhibited by O. tsutsugamushi infection. Beauvericin-induced calcium redistribution was significantly reduced and retarded in cells infected with O. tsutsugamushi. Antiapoptotic activities of O. tsutsugamushi in infected cells are most probably due to inhibition of the increase in the cytosolic calcium concentration.

Effect of calcium on neurohumoral stimulation of feline colonic smooth muscle

1982 ◽  
Vol 243 (2) ◽  
pp. G134-G140
Author(s):  
W. J. Snape
Keyword(s):  
Smooth Muscle ◽  
Spike Activity ◽  
Calcium Ion ◽  
Calcium Concentration ◽  
Extracellular Calcium ◽  
Ion Concentration ◽  
Myoelectric Activity ◽  
Ionic Calcium ◽  
Calcium Ion Concentration ◽  
Stimulation Of

The purpose of this study was to compare the effect of altering the extracellular calcium ion concentration on bethanechol or octapeptide of cholecystokinin (OP-CCK) stimulation of the isolated transverse colon of the cat. Myoelectric activity was recorded with monopolar glass-pore electrodes. Bethanechol (10(-6) M) stimulated an increase in the number of slow waves with superimposed spike potentials to 85.5 +/- 5.3% (P less than 0.001) compared with the basal spike activity (8.9 +/- 1.4%). OP-CCK (4 x 10(-9)) also increased spike activity (80.7 +/- 3.8%, P less than 0.001), which was not inhibited by atropine, phentolamine, or propranolol. Addition of 0.0 mM calcium solution to the colonic smooth muscle abolished both slow-wave and spike activity, which returned after replacing 0.25 mM calcium in the solution. Bethanechol stimulated a greater increase in spike activity as the concentration of calcium was increased. OP-CCK stimulation of colonic spike activity was more sensitive to the extracellular calcium concentration than bethanechol stimulation. Verapamil had a minimal effect on bethanechol stimulation of colonic spike activity, but it inhibited the OP-CCK stimulation. These studies suggest that 1) OP-CCK appears to stimulate colonic smooth muscle directly and 2) OP-CCK requires the presence of a greater amount of extracellular ionic calcium in order to stimulate colonic spike activity compared with bethanechol.

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