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Calcium transient evoked by nicotine in isolated rat vagal pulmonary sensory neurons.

Calcium transient evoked by nicotine in isolated rat vagal pulmonary sensory neurons. Research Abstract Details 

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  • Calcium transient evoked by nicotine in isolated rat vagal pulmonary sensory neurons. Abstract Text:

    jennings xuJennings Xu,wenbin yangWenbin Yang,guangfan zhangGuangfan Zhang,qihai guQihai Gu,lu-yuan leeLu-Yuan Lee,

    It has been shown that inhaled cigarette smoke activates vagal pulmonary C fibers and rapidly adapting receptors (RARs) in the airways and that nicotine contained in the smoke is primarily responsible. This study was carried out to determine whether nicotine alone can activate pulmonary sensory neurons isolated from rat vagal ganglia; the response of these neurons was determined by fura-2-based ratiometric Ca(2+) imaging. The results showed: 1) Nicotine (10(-4) M, 20 s) evoked a transient increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) in 175 of the 522 neurons tested (Delta[Ca(2+)](i) = 142.2 +/- 12.3 nM); the response was reproducible, with a small reduction in peak amplitude in the same neurons when the challenge was repeated 20 min later. 2) A majority (59.7%) of these nicotine-sensitive neurons were also activated by capsaicin (10(-7) M). 3) 1,1-Dimethyl-4-phenylpiperazinium iodide (DMPP; 10(-4) M, 20 s), a selective agonist of the neuronal nicotinic acetylcholine receptors (NnAChRs), evoked a pattern of response similar to that of nicotine. 4) The responses to nicotine and DMPP were either totally abrogated or markedly attenuated by hexamethonium (10(-4) M). 5) In anesthetized rats, right atrial bolus injection of nicotine (75-200 mug/kg) evoked an immediate (latency <1-2 s) and intense burst of discharge in 47.8% of the pulmonary C-fiber endings and 28.6% of the RARs tested. In conclusion, nicotine exerts a direct stimulatory effect on vagal pulmonary sensory nerves, and the effect is probably mediated through an activation of the NnAChRs expressed on the membrane of these neurons.

    Calcium transient evoked by nicotine in isolated rat vagal pulmonary sensory neurons. Publishing Authors By Initials

    j xuJ Xu,w yangW Yang,g zhangG Zhang,q guQ Gu,ly leeLY Lee,

    For similar nervous system: peripheral nervous system: autonomic nervous system: autonomic pathways: vagus nerve research abstracts see: nervous system: peripheral nervous system: autonomic nervous system: autonomic pathways: vagus nerve research

    PUBMED ID PMID:

    MEDLINE DATE:

    Calcium transient evoked by nicotine in isolated rat vagal pulmonary sensory neurons. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: American journal of physiology. Lung cellular and

    VOLUME: 292

    Page Numbers: L54-61

    Journal Abbreviation: Am. J. Physiol. Lung Cell Mol.

    ISSN: 1040-0605

    DAY: 18

    MONTH: 08

    YEAR: 2006

    Calcium transient evoked by nicotine in isolated rat vagal pulmonary sensory neurons. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901229

    Calcium transient evoked by nicotine in isolated rat vagal pulmonary sensory neurons. Keywords Mesh Terms:

    KEYWORDS: Vagus Nerve

    MESH TERMS: physiopathology

    Chemical & Substance for Abstract: Calcium transient evoked by nicotine in isolated rat vagal pulmonary sensory neurons. Information

    Substance Name: Dimethylphenylpiperazinium Iodide

    Registry Number: 54-77-3

    Grant and Affiliation Information for Calcium transient evoked by nicotine in isolated rat vagal pulmonary sensory neurons.

    AFFILIATION: Department of Physiology, University of Kentucky Medical Center, Lexington, KY 40536-0298, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: HL 67379

    ACRONYM: HL

    MEDLINETA: Am J Physiol Lung Cell Mol Phy

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    ACCESSION NUMBER:

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