scholarly journals Regulation of endothelin-1 production by a thromboxane A2 mimetic in rat heart smooth muscle cells

1996 ◽  
Vol 1313 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Chu Chang Chua ◽  
Ronald C. Hamdy ◽  
Balvin H.L. Chua
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Rat Heart ◽  
Thromboxane A2 ◽  
Muscle Cells ◽  
Endothelin 1

Effects of Histamine and Endothelin-1 on Membrane Potentials and Ion Currents in Bovine Tracheal Smooth-Muscle Cells

1998 ◽  
Vol 19 (5) ◽  
pp. 805-811 ◽  
Author(s):  
Masayuki Nara ◽  
Tsukasa Sasaki ◽  
Sanae Shimura ◽  
Takako Oshiro ◽  
Toshiya Irokawa ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Membrane Potentials ◽  
Tracheal Smooth Muscle ◽  
Ion Currents ◽  
Endothelin 1

Actin reorganization in airway smooth muscle cells involves Gq and Gi-2 activation of Rho

1999 ◽  
Vol 277 (3) ◽  
pp. L653-L661 ◽  
Author(s):  
Carol A. Hirshman ◽  
Charles W. Emala
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Actin Polymerization ◽  
Muscle Cells ◽  
Fiber Formation ◽  
Airway Smooth Muscle Cells ◽  
Actin Reorganization ◽  
Endothelin 1 ◽  
In Cells

Extracellular stimuli induce cytoskeleton reorganization (stress-fiber formation) in cells and Ca2+ sensitization in intact smooth muscle preparations by activating signaling pathways that involve Rho proteins, a subfamily of the Ras superfamily of monomeric G proteins. In airway smooth muscle, the agonists responsible for cytoskeletal reorganization via actin polymerization are poorly understood. Carbachol-, lysophosphatidic acid (LPA)-, and endothelin-1-induced increases in filamentous actin staining are indicative of actin reorganization (filamentous-to-globular actin ratios of 2.4 ± 0.3 in control cells, 6.7 ± 0.8 with carbachol, 7.2 ± 0.8 with LPA, and 7.4 ± 0.9 with endothelin-1; P < 0.001; n = 14 experiments). Although the effect of all agonists was blocked by C3 exoenzyme (inactivator of Rho), only carbachol was blocked by pertussis toxin. Although carbachol-induced actin reorganization was blocked in cells pretreated with antisense oligonucleotides directed against Gαi-2 alone, LPA- and endothelin-1-induced actin reorganization were only blocked when both Gαi-2 and Gqα were depleted. These data indicate that in human airway smooth muscle cells, carbachol induces actin reorganization via a Gαi-2pathway, whereas LPA or endothelin-1 induce actin reorganization via either a Gαi-2 or a Gqα pathway.

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.

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