Characterization of 5-Hydroxytryptamine Receptors Mediating Circular Smooth Muscle Contraction in the Human Umbilical Artery

1999 ◽  
Vol 47 (2) ◽  
pp. 102-107 ◽  
Author(s):  
Caroline Karlsson ◽  
Gunilla Bodelsson ◽  
Mikael Bodelsson ◽  
Martin Stjernquist
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Umbilical Artery ◽  
Smooth Muscle Contraction ◽  
Hydroxytryptamine Receptors ◽  
Circular Smooth Muscle ◽  
Human Umbilical Artery

scholarly journals Physiological and pharmacological characterization of transmembrane acid extruders in cultured human umbilical artery smooth muscle cells

2015 ◽  
Vol 35 (5) ◽  
pp. 208
Author(s):  
Shih-Hurng Loh ◽  
Gunng-Shinng Chen ◽  
Ching-Hsia Wu ◽  
Chi-Chiuan Liau ◽  
Chih-Chin Hsu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Umbilical Artery ◽  
Muscle Cells ◽  
Pharmacological Characterization ◽  
Human Umbilical Artery

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.

scholarly journals Characterization of Cecal Smooth Muscle Contraction in Laying Hens

2021 ◽  
Vol 8 (6) ◽  
pp. 91
Author(s):  
Katrin Röhm ◽  
Martin Diener ◽  
Korinna Huber ◽  
Jana Seifert
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Laying Hens ◽  
Ex Vivo ◽  
Isometric Force ◽  
Smooth Muscles ◽  
Smooth Muscle Contraction ◽  
Force Transducer ◽  
Different Levels

The ceca play an important role in the physiology of the gastrointestinal tract in chickens. Nevertheless, there is a gap of knowledge regarding the functionality of the ceca in poultry, especially with respect to physiological cecal smooth muscle contraction. The aim of the current study is the ex vivo characterization of cecal smooth muscle contraction in laying hens. Muscle strips of circular cecal smooth muscle from eleven hens are prepared to investigate their contraction ex vivo. Contraction is detected using an isometric force transducer, determining its frequency, height and intensity. Spontaneous contraction of the chicken cecal smooth muscle and the influence of buffers (calcium-free buffer and potassium-enriched buffer) and drugs (carbachol, nitroprusside, isoprenaline and Verapamil) affecting smooth muscle contraction at different levels are characterized. A decrease in smooth muscle contraction is observed when a calcium-free buffer is used. Carbachol causes an increase in smooth muscle contraction, whereas atropine inhibits contraction. Nitroprusside, isoprenaline and Verapamil result in a depression of smooth muscle contraction. In conclusion, the present results confirm a similar contraction behavior of cecal smooth muscles in laying hens as shown previously in other species.

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.

Cloning and characterization of novel snake venom proteins that block smooth muscle contraction

2002 ◽  
Vol 269 (11) ◽  
pp. 2708-2715 ◽  
Author(s):  
Yasuo Yamazaki ◽  
Hisashi Koike ◽  
Yusuke Sugiyama ◽  
Kazuko Motoyoshi ◽  
Taeko Wada ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Snake Venom ◽  
Smooth Muscle Contraction ◽  
Venom Proteins

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.

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