Effect of antioxidants on airway smooth muscle contraction: action of lipoic acid and some of its novel derivatives on guinea pig tracheal smooth muscle

2009 ◽  
Vol 59 (S2) ◽  
pp. 235-237 ◽  
Author(s):  
E. S. K. Assem ◽  
S. Mann ◽  
B. Y. C. Wan ◽  
C. M. Marson
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Lipoic Acid ◽  
Smooth Muscle Contraction ◽  
Tracheal Smooth Muscle

Role of platelets in contraction of canine tracheal muscle elicited by PAF in vitro

1988 ◽  
Vol 65 (2) ◽  
pp. 914-920 ◽  
Author(s):  
K. J. Popovich ◽  
G. Sheldon ◽  
M. Mack ◽  
N. M. Munoz ◽  
P. Denberg ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Airway Epithelium ◽  
Platelet Activating Factor ◽  
Smooth Muscle Contraction ◽  
Tracheal Smooth Muscle ◽  
Serotonin Antagonist

To elucidate mechanisms of platelet-activating factor (PAF)-induced contraction, we studied the effect of PAF on 203 canine tracheal smooth muscle (TSM) strips from 45 dogs in vitro in the presence and absence of platelets. PAF (10(-11) to 10(-7) M) alone caused no contraction of TSM even in the presence of airway epithelium. In the presence of 2 x 10(5) platelets/microliter, PAF was an extremely potent contractile agonist (threshold 10(-11) M). This response was inhibited by the PAF antagonist, CV-3988 (10(-6) M), and reversed by the serotonin antagonist, methysergide (EC50 = 3.7 +/- 0.79 x 10(-9) M). Neither atropine nor chlorpheniramine (10(-9) to 10(-6) M) attenuated the response to PAF + platelets. In the presence of platelets, 10(-7) M PAF caused an increase in perfusate concentration of serotonin from 0.93 +/- 0.037 x 10(-8) to 1.7 +/- 0.046 x 10(-8) M (P less than 0.001). Tachyphylaxis, previously demonstrated to be irreversible, was shown to be a platelet-dependent phenomenon; contraction could be repeated in the same TSM after addition of fresh platelets. We demonstrate that PAF-induced contraction of canine TSM is caused by the release of cellular intermediates such as serotonin from platelets. We also demonstrate the site of PAF-induced tachyphylaxis in airway smooth muscle contraction.

Blockade of eosinophil migration by 5-lipoxygenase and cyclooxygenase inhibition in explanted guinea pig trachealis

1995 ◽  
Vol 268 (3) ◽  
pp. L446-L454 ◽  
Author(s):  
N. M. Munoz ◽  
A. R. Leff
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Smooth Muscle Contraction ◽  
Cyclooxygenase Inhibition ◽  
Airway Narrowing ◽  
Eosinophil Migration ◽  
Eosinophil Chemotaxis ◽  
Physical Consequences

We studied the effects of 5-lipoxygenase inhibition with A63162 and cyclooxygenase inhibition with indomethacin (INDO) on 1) eosinophil chemotaxis and 2) airway narrowing caused by 10(-6) M formyl-Met-Leu-Phe (fMLP) in tracheal explants from guinea pigs. Airway narrowing was assessed by calibrated micrometry, and eosinophil migration from the lamina propria was expressed as number of eosinophils contained per 1 cm tracheal segment. After 120 min, treatment with fMLP caused an increase in luminal eosinophils from 6,804 +/- 1,786 to 303,347 +/- 75,609 cells (P < 0.001); airway diameter narrowed by 20.4 +/- 1.4%. In six preparations, A63162 inhibited airway narrowing caused by fMLP by 54.9 +/- 6.1%; INDO had a similar effect on airway diameter. However, maximal inhibition of eosinophil migration was greater after 10(-6) M A63162 (38,393 +/- 7,434 cells; P < 0.001 vs. fMLP alone) than after treatment with 10(-5) M INDO (123,547 +/- 19,499 cells; P < 0.05). We demonstrate a method that permits simultaneous measurements of eosinophil migration and airway smooth muscle contraction in a guinea pig tracheal explant preparation. Our data suggest that eosinophil chemotaxis and changes in internal airway diameter are caused by activation of both 5-lipoxygenase and cyclooxygenase pathways and that cell migration is independent of the physical consequences of airway smooth muscle contraction.

scholarly journals The Effect of Auranofine on Tracheal Smooth Muscle Contraction in Guinea Pig.

1993 ◽  
Vol 44 (6) ◽  
pp. 436-448
Author(s):  
Yoshihiko Akiyama ◽  
Tohru Majima ◽  
Michiya Yamaguchi ◽  
Takashi Horie
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscle Contraction ◽  
Smooth Muscle Contraction ◽  
Tracheal Smooth Muscle

Modulation of rate at which serotonin-induced contraction decays in guinea pig trachea

1994 ◽  
Vol 266 (1) ◽  
pp. R221-R227 ◽  
Author(s):  
R. R. Ben-Harari ◽  
B. A. Dalton ◽  
U. C. Garg
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Smooth Muscle Contraction ◽  
Receptor Activation ◽  
Biochemical Pathways ◽  
Biochemical State ◽  
Stimulation Of

Stimulation of the type 2 serotonin (5-HT2) receptor in guinea pig trachea with 5-HT results in a contraction that decays in the continued presence of 5-HT. The decay of the 5-HT contraction has been proposed to be dependent on 5-HT2 receptor activation and to reflect desensitization of the receptor. The characteristics of the decay of the 5-HT contraction may also be dependent on other properties of the tissue. The effects of modulation of biochemical pathways implicated in airway smooth muscle contraction on the 5-HT contraction in isolated guinea pig trachea were determined with the use of a kinetic approach we developed previously. Decay of the 5-HT contraction was inhibited by cooling, increased by forskolin, 3-isobutylmethyl-1-xanthine, and 8-bromoadenosine 3',5'-cyclic monophosphate, and unaffected by staurosporine, H-7, H-8, phorbol 12,13-dibutyrate, and by inhibitors of the three major pathways of arachidonic metabolism. The results suggest that decay of the 5-HT contraction in guinea pig trachea is dependent on both the receptor and the biochemical state of the tissue.

Neutral endopeptidase modulates endothelin-1-induced airway smooth muscle contraction in guinea-pig trachea

1992 ◽  
Vol 39 (2-3) ◽  
pp. 137-145 ◽  
Author(s):  
Giuseppe U. Di Maria ◽  
Michio Katayama ◽  
D.Benjamin Borson ◽  
Jay A. Nadel
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Neutral Endopeptidase ◽  
Smooth Muscle Contraction ◽  
Endothelin 1

Phosphorylation of dense-plaque proteins talin and paxillin during tracheal smooth muscle contraction

1995 ◽  
Vol 268 (3) ◽  
pp. C563-C571 ◽  
Author(s):  
F. M. Pavalko ◽  
L. P. Adam ◽  
M. F. Wu ◽  
T. L. Walker ◽  
S. J. Gunst
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Fold Increase ◽  
Smooth Muscle Contraction ◽  
Tracheal Smooth Muscle ◽  
Airway Smooth Muscle Cells ◽  
Attachment Proteins ◽  
Phosphopeptide Mapping

Reorganization of cytoskeletal-membrane interactions during contractile stimulation may contribute to the regulation of airway smooth muscle contraction. We investigated the effect of contractile stimulation on the phosphorylation of the actin-membrane attachment proteins talin, vinculin, and paxillin. Stimulation of 32P-labeled canine tracheal smooth muscle strips with acetylcholine (ACh; 10(-3) M) resulted in a rapid 2.6-fold increase in phosphorylation of serine and/or threonine residues, compared with resting levels of 0.22 mol PO4(3-)/mol talin. After stimulation with ACh, phosphorylation of tyrosine residues on paxillin increased approximately threefold. Two-dimensional phosphopeptide mapping of in vivo labeled talin and paxillin indicated phosphorylation on a limited number of sites. Vinculin phosphorylation was undetectable in either resting or ACh-stimulated muscle. We conclude that phosphorylation of talin and paxillin occurs during ACh-stimulated contraction of tracheal smooth muscle and that distinct signaling pathways activate a serine/threonine kinase that phosphorylates talin and a tyrosine kinase that phosphorylates paxillin. The pharmacological activation of airway smooth muscle cells might involve the anchoring of contractile filaments to the membrane.

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