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Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves
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| Zeitschriftentitel: | American Journal of Physiology-Lung Cellular and Molecular Physiology |
|---|---|
| Personen und Körperschaften: | , , |
| In: | American Journal of Physiology-Lung Cellular and Molecular Physiology, 268, 1995, 6, S. L950-L956 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Zhang, X. Y. Olszewski, M. A. Robinson, N. E. Zhang, X. Y. Olszewski, M. A. Robinson, N. E. |
|---|---|
| author |
Zhang, X. Y. Olszewski, M. A. Robinson, N. E. |
| spellingShingle |
Zhang, X. Y. Olszewski, M. A. Robinson, N. E. American Journal of Physiology-Lung Cellular and Molecular Physiology Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves Cell Biology Physiology (medical) Pulmonary and Respiratory Medicine Physiology |
| author_sort |
zhang, x. y. |
| spelling |
Zhang, X. Y. Olszewski, M. A. Robinson, N. E. 1040-0605 1522-1504 American Physiological Society Cell Biology Physiology (medical) Pulmonary and Respiratory Medicine Physiology http://dx.doi.org/10.1152/ajplung.1995.268.6.l950 <jats:p> We determined the effects of isoproterenol (Iso) on parasympathetic neurotransmission in isolated equine trachealis strips by comparing the effects of Iso on the contractile response to electrical field stimulation (EFS) and acetylcholine (ACh), as well as by measuring EFS-induced ACh release. The interaction of Iso with muscarinic receptors and endogenous nitric oxide was also investigated. ACh release was measured by high-performance liquid chromatography with electrochemical detection. Iso (10(-7) M or greater) caused significantly more inhibition of EFS- than of ACh-induced contraction, an observation usually interpreted as evidence of prejunctional inhibition of ACh release. However, the latter conclusion was not supported by measurement of ACh release. Iso concentration dependently augmented ACh release, which was reversed by the beta 2-adrenoceptor antagonist ICI-118,551 but not by the beta 1-adrenoceptor antagonist CGP-20,712A. Our results indicate that activation of beta 2-adrenoceptors augments ACh release. Moreover, the comparison of inhibitory effects on EFS- and ACh-induced contraction does not provide correct information about the prejunctional actions of beta-agonists. ACh release was increased more by atropine (10(-7) M) than by Iso (10(-6) M), indicating the predominance of prejunctional inhibitory muscarinic autoreceptors over excitatory beta 2-adrenoceptors. Additionally, we found that inhibition of nitric oxide synthase by NG-nitro-L-arginine did not affect either the cholinergic contractile response or ACh release in both the absence and presence of Iso. </jats:p> Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves American Journal of Physiology-Lung Cellular and Molecular Physiology |
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American Journal of Physiology-Lung Cellular and Molecular Physiology |
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| title |
Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| title_unstemmed |
Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| title_full |
Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| title_fullStr |
Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| title_full_unstemmed |
Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| title_short |
Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| title_sort |
beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| topic |
Cell Biology Physiology (medical) Pulmonary and Respiratory Medicine Physiology |
| url |
http://dx.doi.org/10.1152/ajplung.1995.268.6.l950 |
| publishDate |
1995 |
| physical |
L950-L956 |
| description |
<jats:p> We determined the effects of isoproterenol (Iso) on parasympathetic neurotransmission in isolated equine trachealis strips by comparing the effects of Iso on the contractile response to electrical field stimulation (EFS) and acetylcholine (ACh), as well as by measuring EFS-induced ACh release. The interaction of Iso with muscarinic receptors and endogenous nitric oxide was also investigated. ACh release was measured by high-performance liquid chromatography with electrochemical detection. Iso (10(-7) M or greater) caused significantly more inhibition of EFS- than of ACh-induced contraction, an observation usually interpreted as evidence of prejunctional inhibition of ACh release. However, the latter conclusion was not supported by measurement of ACh release. Iso concentration dependently augmented ACh release, which was reversed by the beta 2-adrenoceptor antagonist ICI-118,551 but not by the beta 1-adrenoceptor antagonist CGP-20,712A. Our results indicate that activation of beta 2-adrenoceptors augments ACh release. Moreover, the comparison of inhibitory effects on EFS- and ACh-induced contraction does not provide correct information about the prejunctional actions of beta-agonists. ACh release was increased more by atropine (10(-7) M) than by Iso (10(-6) M), indicating the predominance of prejunctional inhibitory muscarinic autoreceptors over excitatory beta 2-adrenoceptors. Additionally, we found that inhibition of nitric oxide synthase by NG-nitro-L-arginine did not affect either the cholinergic contractile response or ACh release in both the absence and presence of Iso. </jats:p> |
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| author | Zhang, X. Y., Olszewski, M. A., Robinson, N. E. |
| author_facet | Zhang, X. Y., Olszewski, M. A., Robinson, N. E., Zhang, X. Y., Olszewski, M. A., Robinson, N. E. |
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| description | <jats:p> We determined the effects of isoproterenol (Iso) on parasympathetic neurotransmission in isolated equine trachealis strips by comparing the effects of Iso on the contractile response to electrical field stimulation (EFS) and acetylcholine (ACh), as well as by measuring EFS-induced ACh release. The interaction of Iso with muscarinic receptors and endogenous nitric oxide was also investigated. ACh release was measured by high-performance liquid chromatography with electrochemical detection. Iso (10(-7) M or greater) caused significantly more inhibition of EFS- than of ACh-induced contraction, an observation usually interpreted as evidence of prejunctional inhibition of ACh release. However, the latter conclusion was not supported by measurement of ACh release. Iso concentration dependently augmented ACh release, which was reversed by the beta 2-adrenoceptor antagonist ICI-118,551 but not by the beta 1-adrenoceptor antagonist CGP-20,712A. Our results indicate that activation of beta 2-adrenoceptors augments ACh release. Moreover, the comparison of inhibitory effects on EFS- and ACh-induced contraction does not provide correct information about the prejunctional actions of beta-agonists. ACh release was increased more by atropine (10(-7) M) than by Iso (10(-6) M), indicating the predominance of prejunctional inhibitory muscarinic autoreceptors over excitatory beta 2-adrenoceptors. Additionally, we found that inhibition of nitric oxide synthase by NG-nitro-L-arginine did not affect either the cholinergic contractile response or ACh release in both the absence and presence of Iso. </jats:p> |
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| spelling | Zhang, X. Y. Olszewski, M. A. Robinson, N. E. 1040-0605 1522-1504 American Physiological Society Cell Biology Physiology (medical) Pulmonary and Respiratory Medicine Physiology http://dx.doi.org/10.1152/ajplung.1995.268.6.l950 <jats:p> We determined the effects of isoproterenol (Iso) on parasympathetic neurotransmission in isolated equine trachealis strips by comparing the effects of Iso on the contractile response to electrical field stimulation (EFS) and acetylcholine (ACh), as well as by measuring EFS-induced ACh release. The interaction of Iso with muscarinic receptors and endogenous nitric oxide was also investigated. ACh release was measured by high-performance liquid chromatography with electrochemical detection. Iso (10(-7) M or greater) caused significantly more inhibition of EFS- than of ACh-induced contraction, an observation usually interpreted as evidence of prejunctional inhibition of ACh release. However, the latter conclusion was not supported by measurement of ACh release. Iso concentration dependently augmented ACh release, which was reversed by the beta 2-adrenoceptor antagonist ICI-118,551 but not by the beta 1-adrenoceptor antagonist CGP-20,712A. Our results indicate that activation of beta 2-adrenoceptors augments ACh release. Moreover, the comparison of inhibitory effects on EFS- and ACh-induced contraction does not provide correct information about the prejunctional actions of beta-agonists. ACh release was increased more by atropine (10(-7) M) than by Iso (10(-6) M), indicating the predominance of prejunctional inhibitory muscarinic autoreceptors over excitatory beta 2-adrenoceptors. Additionally, we found that inhibition of nitric oxide synthase by NG-nitro-L-arginine did not affect either the cholinergic contractile response or ACh release in both the absence and presence of Iso. </jats:p> Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves American Journal of Physiology-Lung Cellular and Molecular Physiology |
| spellingShingle | Zhang, X. Y., Olszewski, M. A., Robinson, N. E., American Journal of Physiology-Lung Cellular and Molecular Physiology, Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves, Cell Biology, Physiology (medical), Pulmonary and Respiratory Medicine, Physiology |
| title | Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| title_full | Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| title_fullStr | Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| title_full_unstemmed | Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| title_short | Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| title_sort | beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| title_unstemmed | Beta 2-adrenoceptor activation augments acetylcholine release from tracheal parasympathetic nerves |
| topic | Cell Biology, Physiology (medical), Pulmonary and Respiratory Medicine, Physiology |
| url | http://dx.doi.org/10.1152/ajplung.1995.268.6.l950 |