Role of Ryanodine Receptors in Chloroform-Induced Contraction in Swine Tracheal Smooth Muscle

Lin, Yu; Chen, Hwei-Hsien; Chan, Ming‐Huan

doi:10.1006/taap.2002.9476

Cited by 2 publications

(1 citation statement)

References 33 publications

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“…Ryanodine binds strongly to the RyRs and blocks this Ca 2+ release channels in SR [28], whereas caffeine promotes activation of RyRs and depletes the intracellular Ca 2+ stores [29]. Consistent to our previous report [30], caffeine at 10 mM evoked a contractile response associated with an increase in [Ca 2+ ] i , but ryanodine did not. The SP-induced muscle contraction and Ca 2+ mobilization were significantly reduced by caffeine and fully abolished in the presence with Ca 2+ channel blocker or under withdrawal of external Ca 2+ .…”

Section: Discussionsupporting

confidence: 86%

Involvement of Ca2+ signaling in tachykinin-mediated contractile responses in swine trachea

2005

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Neuropeptide tachykinins, present within sensory nerves, have been implicated as neurotransmitters involved in nonadrenergic and noncholinergic airway muscle contraction. The signal transduction pathways of tachykinins on muscle contraction and Ca2+ mobilization were investigated in swine trachea. Tachykinins, substance P (SP) and neurokinin A (NKA), concentration (1 nM to 1 microM)-dependently induced contractile responses with removal of epithelium, whereas neurokinin B (NKB) did not alter the muscle tension. The SP- and NKA-evoked muscle contractions were inhibited by NK1-R antagonist L732138, but not by either NK2-R antagonist MDL29913 or NK3-R antagonist SB218795. Consistently, SP-elicited increase in [Ca2+]i was abolished by NK1-R antagonist, neither by NK2-R nor NK3-R antagonists. The SP-induced muscular responses were significantly inhibited by L-type Ca2+ channel blocker verapamil and withdrawal of external Ca2+. Caffeine (10 mM) or ryanodine (50 microM) also partly suppressed the SP-induced muscle responses. Inhibition of inositol 1,4,5-trisphosphate (InsP3) receptor with 2-APB (75 microM) potently attenuated SP-evoked Ca2+ mobilization and muscle contraction, which was further inhibited by 2-APB under Ca2+-free external solution, but not completely. Unexpectedly, simultaneous blockade of InsP3 receptor and ryanodine receptor (RyR) by 2-APB and ryanodine enhanced SP-evoked muscle contraction and Ca2+ mobilization. This potentiation was virtually abolished by removal of external Ca2+, suggesting native Ca2+ channels may contribute to this phenomenon. These results demonstrate that tachykinins produce a potent muscle contraction associated with Ca2+ mobilization via tachykinin NK1- R-dependent activation of multiple signal transduction pathways involving Ca2+ influx and release of Ca2+ from InsP3- and ryanodine-sensitive Ca2+ stores. Blockade of both InsP3 receptor and RyR enhances the Ca2+ influx through native Ca2+ channels in plasma membrane, which is crucial to Ca2+ signaling in response to NK1 receptor activation.

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Section: Discussionsupporting

confidence: 86%

Involvement of Ca2+ signaling in tachykinin-mediated contractile responses in swine trachea

2005

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Effects of Trichloroethylene and Perchloroethylene on Muscle Contractile Responses and Epithelial Prostaglandin Release and Acetylcholinesterase Activity in Swine Trachea

Chen

Lin²,

Peng³

et al. 2004

Toxicological Sciences

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Trichloroethylene (TCE) and perchloroethylene (PERC) have been reported to induce respiratory complications such as airway hyperactivity and asthma. The present study was designed to investigate their influence on smooth muscle contraction and epithelial release of prostanoids in swine trachea. Results showed that TCE and PERC exposure did not alter the basal tone of tracheal smooth muscle. However, TCE and PERC concentration-dependently increased both ACh-induced and high K+-induced muscle contraction. In addition to potentiation of muscle contractile responses evoked by acetylcholine or histamine, pretreatment of smooth muscle with PERC at higher concentration significantly suppressed the relaxant activity of beta-adrenergic agonists. The epithelial prostaglandin (PG)E2, but not PGD2, release from tracheal epithelium was significantly increased by TCE and PERC. In addition, the acetylcholinesterse (AChE) activity of tracheal epithelia was reduced by TCE and PERC. In conclusion, our results suggest that the enhancement of spasmogen-evoked muscle contractile responses and epithelial PGE2 secretion, as well as reduction of epithelial AChE activity, may participate in airway impairment and hyperresponsiveness after TCE and PERC exposure.

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Role of Ryanodine Receptors in Chloroform-Induced Contraction in Swine Tracheal Smooth Muscle

Cited by 2 publications

References 33 publications

Involvement of Ca2+ signaling in tachykinin-mediated contractile responses in swine trachea

Involvement of Ca2+ signaling in tachykinin-mediated contractile responses in swine trachea

Effects of Trichloroethylene and Perchloroethylene on Muscle Contractile Responses and Epithelial Prostaglandin Release and Acetylcholinesterase Activity in Swine Trachea

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