J Physiol Wellcome Trust-funded researchers
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Physiol Vol 349 pp 553-570
Copyright © 1984 by The Physiological Society
This Article
Right arrow Full Text (PDF)
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Inoue, T
Right arrow Articles by Takeda, K
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Inoue, T
Right arrow Articles by Takeda, K

Prostaglandin-induced inhibition of acetylcholine release from neuronal elements of dog tracheal tissue.

T Inoue, Y Ito and K Takeda

In an attempt to elucidate the possible roles of endogenous prostaglandins on the neuro-effector transmission in the dog trachea, effects of a prostaglandin antagonist (1-acetyl-2-[8-chloro-10, 11- dihydrobenz (b.f) (1.4) oxazepine-10-carbonyl]hydrazine (SC-19220] on the electrical and mechanical properties of smooth muscle cells and on neuro-effector transmission in the smooth muscle layer were studied by means of micro-electrode, double sucrose-gap, and tension recording methods. The levels of prostaglandins in the perfusate from the dog tracheal tissue were also determined using radioimmunoassay. Excitatory junction potentials (e.j.p.s) and twitch tension evoked by electrical field stimulation with short pulse duration (50-100 microseconds), which were abolished by tetrodotoxin (10(-7) M) or atropine (5 X 10(-6) M), showed gradual and continuous reduction in amplitude during superfusion with normal Krebs solution. Reduction in the amplitude of e.j.p.s occurred with no change in the membrane potential or membrane input resistance. SC-19220 (3.1 X 10(-5) M) did not modify the membrane potential, membrane input resistance or the sensitivity to acetylcholine of the smooth muscle cells. Yet, with application of SC-19220 (3.1 X 10(-6) M), gradual and continuous reductions in the amplitude of e.j.p.s and twitch contractions were no longer observed. With an increased concentration (3.1 X 10(-5) M), e.j.p.s and twitch contractions with a constant amplitude were obtained after the initial increase in the amplitude. When the amplitude of twitch contractions was stabilized by treatment with indomethacin (10(-5) M), low concentrations (10(-12) to 10(-10) M) of prostaglandin E2 (PGE2) or prostaglandin F2 alpha (10(-8) to 10(-6) M) markedly suppressed the amplitude of the twitch contractions. In some muscle preparations (ten out of twenty-two preparations examined), SC-19220 (3.1 X 10(-6) to 3.1 X 10(-5) M) produced a sustained contraction of the muscle, which was suppressed by atropine (5 X 10(-6) M) or PGE2 (10(-8) M). Following pre-treatment of the tissue with atropine (5 X 10(-6) M), SC-19220 did not evoke contracture. In the resting condition, 10-40 ng g-1 wet wt. tissue min-1 PGE or PGF was released into the perfusate from the tracheal muscle tissue of the control dog.(ABSTRACT TRUNCATED AT 400 WORDS)




This article has been cited by other articles:


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
R. Kajekar, B. J. Undem, and A. C. Myers
Role of cyclooxygenase activation and prostaglandins in antigen-induced excitability changes of bronchial parasympathetic ganglia neurons
Am J Physiol Lung Cell Mol Physiol, April 1, 2003; 284(4): L581 - L587.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1984 The Physiological Society.