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Effects of prolonged exposure to α,β‐methylene ATP on non‐adrenergic, non‐cholinergic excitatory transmission in the rectum of the chicken
Author(s) -
Komori Seiichi,
Kwon SeongChun,
Ohashi Hidenori
Publication year - 1988
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1988.tb11494.x
Subject(s) - adrenergic , excitatory postsynaptic potential , rectum , cholinergic , chemistry , endocrinology , transmission (telecommunications) , neuroscience , medicine , biology , inhibitory postsynaptic potential , computer science , receptor , telecommunications
1 Effects of prolonged exposure to α,β‐methylene ATP (α,β‐Me ATP) on contractions and excitatory junction potentials (e.j.ps) evoked by non‐adrenergic, non‐cholinergic (NANC) excitatory nerve stimulation have been investigated in the chicken isolated rectum and longitudinal muscle strip from chicken rectum pretreated with atropine (0.5 μ m ), methysergide (2 μ m ) and pyrilamine (3 μ m ). 2 α,β‐Me ATP (20 n m ‐4 μ m ) caused a rapid rise in tension of the longitudinal muscle of the isolated rectum preparation which returned to the baseline levels after a few minutes. The magnitude of the contractile response to NANC nerve stimulation was reduced after exposure to the drug. The inhibitory effect was related to the drug concentration; at 4 μ m the nerve‐mediated contraction was abolished and frequently converted to a relaxation. 3 Adenosine 5′‐triphosphate (ATP, 100 μ m ), bovine neurotensin (2.5 n m ) and K + ‐rich solutions (30 m m and 60 m m ) all produced a transient contraction of the isolated rectum preparation. The exposure to α,β‐Me ATP (0.2 and 4 μ m ) also rendered the preparation less sensitive to these stimulant substances. 4 α,β‐Me ATP (0.2 and 4 μ m caused a membrane depolarization in cells of the longitudinal muscle strip. The depolarization reached a peak within 2–3 min after application and then decayed to a steady level that was still more positive than the baseline level. The electrotonic potentials were reduced in amplitude to 44 ± 8% ( n = 7) of the normal amplitude if measured at the peak depolarization produced with 0.2 μ m α,β‐Me ATP, and to 62 ± 10% ( n = 7) if measured at the steady‐state depolarization. With 4 μ m , the corresponding percentages were 33 ± 7% ( n = 8) and 55 ± 7% ( n = 8), indicating a decrease in membrane resistance. 5 The e.j.ps in response to field stimulation of the intramural nerves and Remak's nerve stimulation were decreased in amplitude and duration during exposure to α,β‐Me ATP (0.2 and 4 μ m ). 6 The smooth muscle cells regained normal membrane resistance and sensitivity to ATP on washout of α,β‐Me ATP (4 μ m ) more rapidly than the responses to NANC nerve stimulation. 7 It can be argued from the results that the suppression by α,β‐Me ATP of the contraction and e.j.p. evoked by NANC nerve stimulation in the chicken rectum, unlike the mammalian preparations described previously, is due mainly to a change in the electrical properties of the membrane of the smooth muscle cells, rather than being due, or only partly due, to desensitization of the purine receptor.