scholarly journals Inhibitory Effects of Dantrolene on Contractile Responses in Gastric Smooth Muscle of the Rat.

1994 ◽  
Vol 56 (2) ◽  
pp. 275-279 ◽  
Author(s):  
Kimihiko SATOH ◽  
Toshio OHTA ◽  
Shigeo ITO ◽  
Yoshikazu NAKAZATO
Keyword(s):  
Smooth Muscle ◽  
Inhibitory Effects ◽  
Contractile Responses ◽  
Gastric Smooth Muscle

scholarly journals Adiponectin Exerts Peripheral Inhibitory Effects on the Mouse Gastric Smooth Muscle through the AMPK Pathway

2020 ◽  
Vol 21 (24) ◽  
pp. 9617
Author(s):  
Eglantina Idrizaj ◽  
Rachele Garella ◽  
Silvia Nistri ◽  
Alfonso Dell’Accio ◽  
Emanuele Cassioli ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Multidisciplinary Approach ◽  
Gastric Fundus ◽  
Inhibitory Effects ◽  
Immunofluorescence Analysis ◽  
Synthesis Inhibitor ◽  
Ampk Signaling ◽  
Gastric Smooth Muscle ◽  
Treatment Of Obesity ◽  
Amp Activated Protein Kinase

Some adipokines, such as adiponectin (ADPN), other than being implicated in the central regulation of feeding behavior, may influence gastric motor responses, which are a source of peripheral signals that also influence food intake. The present study aims to elucidate the signaling pathways through which ADPN exerts its actions in the mouse gastric fundus. To this purpose, we used a multidisciplinary approach. The mechanical results showed that ADPN caused a decay of the strip basal tension, which was abolished by the nitric oxide (NO) synthesis inhibitor, L-NG-nitro arginine (L-NNA). The electrophysiological experiments confirmed that all ADPN effects were abolished by L-NNA, except for the reduction of Ca2+ current, which was instead prevented by the inhibitor of AMP-activated protein kinase (AMPK), dorsomorphin. The activation of the AMPK signaling by ADPN was confirmed by immunofluorescence analysis, which also revealed the ADPN R1 receptor (AdipoR1) expression in glial cells of the myenteric plexus. In conclusion, our results indicate that ADPN exerts an inhibitory action on the gastric smooth muscle by acting on AdipoR1 and involving the AMPK signaling pathway at the peripheral level. These findings provide novel bases for considering AMPK as a possible pharmacologic target for the potential treatment of obesity and eating disorders.

scholarly journals Inhibition of RhoA-dependent pathway and contraction by endogenous hydrogen sulfide in rabbit gastric smooth muscle cells

2015 ◽  
Vol 308 (6) ◽  
pp. C485-C495 ◽  
Author(s):  
Ancy D. Nalli ◽  
Senthilkumar Rajagopal ◽  
Sunila Mahavadi ◽  
John R. Grider ◽  
Karnam S. Murthy
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Contraction ◽  
Light Chain ◽  
Rho Kinase ◽  
Muscle Cells ◽  
Inhibitory Effects ◽  
Gastric Smooth Muscle ◽  
Camp And Cgmp ◽  
Cgmp Formation

Inhibitory neurotransmitters, chiefly nitric oxide and vasoactive intestinal peptide, increase cyclic nucleotide levels and inhibit muscle contraction via inhibition of myosin light chain (MLC) kinase and activation of MLC phosphatase (MLCP). H2S produced as an endogenous signaling molecule synthesized mainly from l-cysteine via cystathionine-γ-lyase (CSE) and cystathionine-β-synthase (CBS) regulates muscle contraction. The aim of this study was to analyze the expression of CSE and H2S function in the regulation of MLCP activity, 20-kDa regulatory light chain of myosin II (MLC20) phosphorylation, and contraction in isolated gastric smooth muscle cells. Both mRNA expression and protein expression of CSE, but not CBS, were detected in smooth muscle cells of rabbit, human, and mouse stomach. l-cysteine, an activator of CSE, and NaHS, a donor of H2S, inhibited carbachol-induced Rho kinase and PKC activity, Rho kinase-sensitive phosphorylation of MYPT1, PKC-sensitive phosphorylation of CPI-17, and MLC20 phosphorylation and sustained muscle contraction. The inhibitory effects of l-cysteine, but not NaHS, were blocked upon suppression of CSE expression by siRNA or inhibition of its activity by dl-propargylglycine (PPG) suggesting that the effect of l-cysteine is mediated via activation of CSE. Glibenclamide, an inhibitor of KATP channels, had no effect on the inhibition of contraction by H2S. Both l-cysteine and NaHS had no effect on basal cAMP and cGMP levels but augmented forskolin-induced cAMP and SNP-induced cGMP formation. We conclude that both endogenous and exogenous H2S inhibit muscle contraction, and the mechanism involves inhibition of Rho kinase and PKC activities and stimulation of MLCP activity leading to MLC20 dephosphorylation and inhibition of muscle contraction.

Effects of extracellular calcium on canine tracheal smooth muscle

1986 ◽  
Vol 61 (2) ◽  
pp. 706-711 ◽  
Author(s):  
S. J. Gunst ◽  
J. M. Pisoni
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Extracellular Calcium ◽  
Tracheal Smooth Muscle ◽  
Inhibitory Effects ◽  
Contractile Responses ◽  
Low Concentrations ◽  
K Depletion

Strips of canine tracheal smooth muscle were studied in vitro to determine the effects of changes in the extracellular calcium (Cao) concentration on tonic contractions induced by acetylcholine and 5-hydroxytryptamine. Strips were contracted with graded concentrations of the above agents in 2.4 mM Ca, after which CaCl2 was administered to achieve final concentrations of 5.0, 10.0, and 20.0 mM. Increases in Cao to 5 mM or above caused significant relaxation of muscles contracted with 5-hydroxytryptamine but did not significantly relax muscles contracted with acetylcholine. Increases in Cao also caused significant relaxation of muscles contracted with low concentrations of K+ (20 or 30 mM). However, in 60 or 120 mM K+, increases in Cao resulted predominantly in muscle contraction. Inhibition of the Na+-K+-ATPase by ouabain (10(-5) M) or K+ depletion reversed the effects of Cao from relaxation to contraction in tissues contracted with 5-hydroxytryptamine. Increases in Cao also caused contraction rather than relaxation in the presence of verapamil (10(-6) M). We conclude that calcium has both excitatory and inhibitory effects on the contractile responses of canine tracheal smooth muscle. The inhibitory effects of Ca2+ appear to be linked to the activity of the membrane Na+-K+-ATPase.

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