Mediation of anaphylaxis-induced jejunal circular smooth muscle contraction in rats

1993 ◽  
Vol 38 (3) ◽  
pp. 396-402 ◽  
Author(s):  
R. B. Scott ◽  
M. Maric
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Smooth Muscle Contraction ◽  
Circular Smooth Muscle

Involvement of the Tyr Kinase/JNK Pathway in Carbachol-induced Bronchial Smooth Muscle Contraction in the Rat

2013 ◽  
Vol 118 (5) ◽  
pp. 1076-1085 ◽  
Author(s):  
Hiroyasu Sakai ◽  
Yu Watanabe ◽  
Mai Honda ◽  
Rika Tsuiki ◽  
Yusuke Ueda ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Kinase Inhibitors ◽  
Smooth Muscles ◽  
Smooth Muscle Contraction ◽  
Organ Bath ◽  
Bronchial Smooth Muscle ◽  
Jnk Pathway ◽  
Circular Smooth Muscle ◽  
Mitogen Activated Protein

Abstract Background: Tyrosine (Tyr) kinases and mitogen-activated protein kinases have been thought to participate in the contractile response in various smooth muscles. The aim of the current study was to investigate the involvement of the Tyr kinase pathway in the contraction of bronchial smooth muscle. Methods: Ring preparations of bronchi isolated from rats were suspended in an organ bath. Isometric contraction of circular smooth muscle was measured. Immunoblotting was used to examine the phosphorylation of c-Jun N-terminal kinasess (JNKs) in bronchial smooth muscle. Results: To examine the role of mitogen-activated protein kinase(s) in bronchial smooth muscle contraction, the effects of MPAK inhibitors were investigated in this study. The contraction induced by carbachol (CCh) was significantly inhibited by pretreatment with selective Tyr kinase inhibitors (genistein and ST638, n = 6, respectively), and a JNK inhibitor (SP600125, n = 6). The contractions induced by high K+ depolarization (n = 4), orthovanadate (a potent Tyr phosphatase inhibitor) and sodium fluoride (a G protein activator; NaF) were also significantly inhibited by selective Tyr kinase inhibitors and a JNK inhibitor (n = 4, respectively). However, the contraction induced by calyculin-A was not affected by SP600125. On the other hand, JNKs were phosphorylated by CCh (2.2 ± 0,4 [mean±SEM] fold increase). The JNK phosphorylation induced by CCh was significantly inhibited by SP600125 (n = 4). Conclusion: These findings suggest that the Tyr kinase/JNK pathway may play a role in bronchial smooth muscle contraction. Strategies to inhibit JNK activation may represent a novel therapeutic approach for diseases involving airway obstruction, such as asthma and chronic obstructive pulmonary disease.

Role of cADPR in sodium nitroprusside-induced opossum esophageal longitudinal smooth muscle contraction

2007 ◽  
Vol 292 (6) ◽  
pp. G1543-G1548 ◽  
Author(s):  
R. K. Campbell ◽  
R. W. Wells ◽  
D. V. Miller ◽  
W. G. Paterson
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Sodium Nitroprusside ◽  
Smooth Muscle Contraction ◽  
Isometric Tension ◽  
Circular Smooth Muscle ◽  
Longitudinal Smooth Muscle ◽  
Second Messenger Pathways ◽  
Opposing Effects

Nitric oxide (NO) relaxes most smooth muscle, including the circular smooth muscle (CSM) of the esophagus, whereas in the adjacent longitudinal smooth muscle (LSM), it causes contraction. The second messenger pathways responsible for this NO-induced LSM contraction are unclear, given that these opposing effects of NO are both cGMP dependent. In intestinal LSM, but not CSM, cADP ribose (cADPR)-dependent pathways participate in Ca2+ mobilization and muscle contraction; whether similar differences exist in the esophagus is unknown. The purpose of this study was to determine whether cADPR plays a role in the NO-mediated contraction of opossum esophageal LSM. Standard isometric tension recordings were performed using both LSM and CSM strips from opossum distal esophagus that were hung in 10-ml tissue baths perfused with oxygenated Krebs solution. cADPR produced concentration-dependent contraction of LSM strips with an EC50 of 1 nM and peak contraction of 57 ± 18% of the 60 mM KCl-induced contraction. cADPR had no effect on CSM strips at concentrations up to 10−6 M. The EC50 of cADPR caused contraction (18 ± 2% from initial resting length) of isolated LSM cells. Sodium nitroprusside (SNP; 300 μM) induced contraction of LSM strips that averaged 67 ± 5% of the KCl response. cADPR antagonists 8-bromo-cADPR and 8-amino-cADPR, as well as ryanodine receptor antagonists ryanodine and tetracaine, significantly inhibited the SNP-induced contraction. In conclusion, in the opossum esophagus, 1) cADPR induces contraction of LSM, but not CSM, and 2) NO-induced contraction of LSM appears to involve a cADPR-dependent pathway.

Role of sodium or calcium in electrical depolarization of feline colonic smooth muscle

1985 ◽  
Vol 249 (1) ◽  
pp. G66-G72 ◽  
Author(s):  
W. J. Snape ◽  
S. T. Tan
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Muscle Contraction ◽  
Muscle Tension ◽  
Smooth Muscle Contraction ◽  
Extracellular Calcium ◽  
Resting Potential ◽  
Spike Potential ◽  
Circular Smooth Muscle

The aim of this study was to compare the role of Na+ and Ca2+ on the membrane potential and contraction of feline colonic circular smooth muscle. The changes in membrane potential were correlated with a change in tension using the double-sucrose gap technique. The estimated resting potential was -62.8 +/- 2.6 mV. A depolarizing current, passed during quiescent periods of the membrane, stimulated a spike potential and caused a concomitant increase in smooth muscle tension. The maximum depolarization rate of the active spike potential was rapid (580 +/- 75 mV/s) and unaffected by the amplitude of the depolarizing current. Reduction of extracellular calcium (0.0 mM Ca2+ plus 5 mM EGTA) or blockade of the calcium channels with verapamil (10(-6)M) slowed the maximum rate of membrane depolarization to 128 +/- 20 mV/s (P less than 0.001). The steady-state amplitude of the electrotonic potential and time constant also decreased in low-calcium solutions. The amplitude of smooth muscle contraction and the time between stimulus and onset of contraction were dependent on the amplitude of the depolarizing current and the concentration of extracellular calcium. Removal of sodium had no effect on the electrotonic potentials, maximum dV/dt of the spike, or the contraction of the smooth muscle. These studies suggest calcium plays a major role in the generation of an active spike potential, colonic smooth muscle contraction requires extracellular calcium and is associated with an active regenerative spike potential, and sodium plays a minor role in the generation of an active spike potential and in the initiation of a contraction in feline colonic smooth muscle.

scholarly journals Reduced biomechanical models for precision-cut lung-slice stretching experiments

2021 ◽  
Vol 82 (5) ◽  
Author(s):  
Hannah J. Pybus ◽  
Amanda L. Tatler ◽  
Lowell T. Edgar ◽  
Reuben D. O’Dea ◽  
Bindi S. Brook
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Ex Vivo ◽  
Finite Thickness ◽  
Biomechanical Model ◽  
Local Stress ◽  
Smooth Muscle Contraction ◽  
Biomechanical Models ◽  
Cytokine Activation ◽  
Asymptotic Reduction

AbstractPrecision-cut lung-slices (PCLS), in which viable airways embedded within lung parenchyma are stretched or induced to contract, are a widely used ex vivo assay to investigate bronchoconstriction and, more recently, mechanical activation of pro-remodelling cytokines in asthmatic airways. We develop a nonlinear fibre-reinforced biomechanical model accounting for smooth muscle contraction and extracellular matrix strain-stiffening. Through numerical simulation, we describe the stresses and contractile responses of an airway within a PCLS of finite thickness, exposing the importance of smooth muscle contraction on the local stress state within the airway. We then consider two simplifying limits of the model (a membrane representation and an asymptotic reduction in the thin-PCLS-limit), that permit analytical progress. Comparison against numerical solution of the full problem shows that the asymptotic reduction successfully captures the key elements of the full model behaviour. The more tractable reduced model that we develop is suitable to be employed in investigations to elucidate the time-dependent feedback mechanisms linking airway mechanics and cytokine activation in asthma.

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