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Articles in PresS, published online ahead of print April 11, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00001.2002
Submitted on January 7, 2002
Accepted on March 17, 2002
1 Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
2 Department of Pharmacology, Kings College, London, United Kingdom
3 Department of Pharmacology, Univ. of California at Davis, Davis, California, USA
* To whom correspondence should be addressed. E-mail: bjc{at}jhmi.edu.
Neurokinin-containing nerve fibers were localized to guinea pig airway parasympathetic ganglia in control tissues but not in tissues pretreated with capsaicin. The purpose of the present study was to determine if neurokinins, released during axonal reflexes or following antidromic afferent nerve stimulation, modulate ganglionic synaptic neurotransmission. The NK3 receptor antagonists SB223412 and SR142801 inhibited vagally-mediated cholinergic contractions of bronchi in vitro at stimulation voltages threshold for preganglionic nerve activation, but had no effect on vagally-mediated contractions evoked at optimal voltage or field stimulation-induced contractions. Intracellular recordings from the ganglia neurons revealed that capsaicin-sensitive nerve stimulation potentiated subsequent preganglionic nerve-evoked fast excitatory post-synaptic potentials. This effect was mimicked by the NK3 receptor agonist senktide analog and blocked SB223412. In situ, senktide analog markedly increased baseline tracheal cholinergic tone, an effect that was reversed by atropine and prevented by vagotomy or SB223412. Comparable effects of intravenous senktide analog on pulmonary insufflation pressure were observed. These data highlight the important integrative role played by parasympathetic ganglia and indicate that activation of NK3 receptors in airway ganglia by endogenous neurokinins facilitates synaptic neurotransmission.
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