Modulation of equine tracheal smooth muscle contractility by epithelial-derived and cyclooxygenase metabolites

Gussie J. Tessier; Petra A. Lackner; Scott M O'Grady; Mathur S Kannan

doi:10.1016/0034-5687(91)90022-B

Modulation of equine tracheal smooth muscle contractility by epithelial-derived and cyclooxygenase metabolites

Gussie J. Tessier, Petra A. Lackner, Scott M O'Grady, Mathur S Kannan

Research output: Contribution to journal › Article › peer-review

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Abstract

The role of epithelium in the modulation of contractile responses to electrical field stimulation (EFS), acetylcholine (ACh), and KCl were studied in vitro in strips of equine tracheal smooth muscle (TSM). EFS with 0.5 ms pulses of voltage (70 V) resulted in frequency dependent contractions of equine TSM that were sensitive to tetrodotoxin (TTX) and atropine. In TSM without epithelium, preincubation with indomethacin significantly potentiated contractile responses to EFS. The potentiating effect of indomethacin on EFS contractions was abolished by the addition of 3 nM prostaglandin E₂ (PGE₂). ACh and KCl cumulative concentration-response curves were shifted to the left by removal of epithelium from equine TSM strips with a significant decrease in the 50% effective concentration (EC₅₀) for both ACh and KCl. The mean EC₅₀ (± SE) for ACh in TSM without epithelium was 0.51 ± 0.09 μM vs 4.30 ± 1.03 μM in TSM with epithelium. Similarly, the mean EC₅₀ (± SE) for KCl in TSM without epithelium was 22.20 ± 2.61 mM vs 32.35 ± 2.66 mM in TSM with epithelium. The addition of indomethacin (3 μM) had no effect on the ACh concentration-response curves in TSM strips with or without epithelium. Our results suggest that in the equine airway there is (1) an epithelial-derived relaxant factor that modulates tracheal smooth muscle contractility postsynaptically, and (2) a nonepithelial-derived inhibitory factor, possibly PGE₂, that modulates ACh release from nerves presynaptically.

Original language	English (US)
Pages (from-to)	105-114
Number of pages	10
Journal	Respiration Physiology
Volume	84
Issue number	1
DOIs	https://doi.org/10.1016/0034-5687(91)90022-B
State	Published - Apr 1991

Bibliographical note

Funding Information:
Support Grant from the NIH. We, especially want to thank Dr David R. Brown for helpful discussions and Dr Brad Gordon for his help and support. We also wish to thank Dr Vic Cox, Jim Malone, Duane Weiss and members of the Large Animal Clinical Sciences department for their help with this project. Petra Lackner was recipient of a UROP award from, the University of Minnesota.

Funding Information:
Acknowledgements.T his work was supported by the Cystic Fibrosis Foundation and a Biomedical Research

Keywords

Prostaglandin, and tracheal smooth muscle
Tracheal smooth muscle

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10.1016/0034-5687(91)90022-B

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title = "Modulation of equine tracheal smooth muscle contractility by epithelial-derived and cyclooxygenase metabolites",

abstract = "The role of epithelium in the modulation of contractile responses to electrical field stimulation (EFS), acetylcholine (ACh), and KCl were studied in vitro in strips of equine tracheal smooth muscle (TSM). EFS with 0.5 ms pulses of voltage (70 V) resulted in frequency dependent contractions of equine TSM that were sensitive to tetrodotoxin (TTX) and atropine. In TSM without epithelium, preincubation with indomethacin significantly potentiated contractile responses to EFS. The potentiating effect of indomethacin on EFS contractions was abolished by the addition of 3 nM prostaglandin E2 (PGE2). ACh and KCl cumulative concentration-response curves were shifted to the left by removal of epithelium from equine TSM strips with a significant decrease in the 50% effective concentration (EC50) for both ACh and KCl. The mean EC50 (± SE) for ACh in TSM without epithelium was 0.51 ± 0.09 μM vs 4.30 ± 1.03 μM in TSM with epithelium. Similarly, the mean EC50 (± SE) for KCl in TSM without epithelium was 22.20 ± 2.61 mM vs 32.35 ± 2.66 mM in TSM with epithelium. The addition of indomethacin (3 μM) had no effect on the ACh concentration-response curves in TSM strips with or without epithelium. Our results suggest that in the equine airway there is (1) an epithelial-derived relaxant factor that modulates tracheal smooth muscle contractility postsynaptically, and (2) a nonepithelial-derived inhibitory factor, possibly PGE2, that modulates ACh release from nerves presynaptically.",

keywords = "Prostaglandin, and tracheal smooth muscle, Tracheal smooth muscle",

author = "Tessier, {Gussie J.} and Lackner, {Petra A.} and O'Grady, {Scott M} and Kannan, {Mathur S}",

note = "Funding Information: Support Grant from the NIH. We, especially want to thank Dr David R. Brown for helpful discussions and Dr Brad Gordon for his help and support. We also wish to thank Dr Vic Cox, Jim Malone, Duane Weiss and members of the Large Animal Clinical Sciences department for their help with this project. Petra Lackner was recipient of a UROP award from, the University of Minnesota. Funding Information: Acknowledgements.T his work was supported by the Cystic Fibrosis Foundation and a Biomedical Research",

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N1 - Funding Information: Support Grant from the NIH. We, especially want to thank Dr David R. Brown for helpful discussions and Dr Brad Gordon for his help and support. We also wish to thank Dr Vic Cox, Jim Malone, Duane Weiss and members of the Large Animal Clinical Sciences department for their help with this project. Petra Lackner was recipient of a UROP award from, the University of Minnesota. Funding Information: Acknowledgements.T his work was supported by the Cystic Fibrosis Foundation and a Biomedical Research

PY - 1991/4

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N2 - The role of epithelium in the modulation of contractile responses to electrical field stimulation (EFS), acetylcholine (ACh), and KCl were studied in vitro in strips of equine tracheal smooth muscle (TSM). EFS with 0.5 ms pulses of voltage (70 V) resulted in frequency dependent contractions of equine TSM that were sensitive to tetrodotoxin (TTX) and atropine. In TSM without epithelium, preincubation with indomethacin significantly potentiated contractile responses to EFS. The potentiating effect of indomethacin on EFS contractions was abolished by the addition of 3 nM prostaglandin E2 (PGE2). ACh and KCl cumulative concentration-response curves were shifted to the left by removal of epithelium from equine TSM strips with a significant decrease in the 50% effective concentration (EC50) for both ACh and KCl. The mean EC50 (± SE) for ACh in TSM without epithelium was 0.51 ± 0.09 μM vs 4.30 ± 1.03 μM in TSM with epithelium. Similarly, the mean EC50 (± SE) for KCl in TSM without epithelium was 22.20 ± 2.61 mM vs 32.35 ± 2.66 mM in TSM with epithelium. The addition of indomethacin (3 μM) had no effect on the ACh concentration-response curves in TSM strips with or without epithelium. Our results suggest that in the equine airway there is (1) an epithelial-derived relaxant factor that modulates tracheal smooth muscle contractility postsynaptically, and (2) a nonepithelial-derived inhibitory factor, possibly PGE2, that modulates ACh release from nerves presynaptically.

AB - The role of epithelium in the modulation of contractile responses to electrical field stimulation (EFS), acetylcholine (ACh), and KCl were studied in vitro in strips of equine tracheal smooth muscle (TSM). EFS with 0.5 ms pulses of voltage (70 V) resulted in frequency dependent contractions of equine TSM that were sensitive to tetrodotoxin (TTX) and atropine. In TSM without epithelium, preincubation with indomethacin significantly potentiated contractile responses to EFS. The potentiating effect of indomethacin on EFS contractions was abolished by the addition of 3 nM prostaglandin E2 (PGE2). ACh and KCl cumulative concentration-response curves were shifted to the left by removal of epithelium from equine TSM strips with a significant decrease in the 50% effective concentration (EC50) for both ACh and KCl. The mean EC50 (± SE) for ACh in TSM without epithelium was 0.51 ± 0.09 μM vs 4.30 ± 1.03 μM in TSM with epithelium. Similarly, the mean EC50 (± SE) for KCl in TSM without epithelium was 22.20 ± 2.61 mM vs 32.35 ± 2.66 mM in TSM with epithelium. The addition of indomethacin (3 μM) had no effect on the ACh concentration-response curves in TSM strips with or without epithelium. Our results suggest that in the equine airway there is (1) an epithelial-derived relaxant factor that modulates tracheal smooth muscle contractility postsynaptically, and (2) a nonepithelial-derived inhibitory factor, possibly PGE2, that modulates ACh release from nerves presynaptically.

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ER -

Modulation of equine tracheal smooth muscle contractility by epithelial-derived and cyclooxygenase metabolites

Abstract

Bibliographical note

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