Contractile and phosphatidylinositol responses of rat trachea to anticholinesterase drugs
Contractile and phosphatidylinositol responses of rat trachea to anticholinesterase drugs
复制标题
大鼠气管对抗胆碱酯酶药物的收缩和磷脂酰肌醇反应
DOI:
10.1007/bf03012462
复制
发表时间:
1998
期刊:
影响因子:
--
通讯作者:
K. Sumikawa
中科院分区:
文献类型:
--
作者:
O. Shibata;A. Tsuda;T. Makita;Shunichiro Iwanaga;T. Hara;S. Shibata;K. Sumikawa
PurposeSome anticholinesterases (anti-ChE) such as neostigmine and pyridostigmine but not edrophonium, stimulate phosphatidylinositol (PI) response. Although a direct relationship was suggested between the increase in PI response and airway smooth muscle contraction, there are no data regarding the effects of anti-ChE drugs on airway smooth muscle. Thus, we examined the contractile properties and PI responses produced by anti-ChE drugs.MethodsContractile response. Rat tracheal ring was suspended between two stainless hooks in Krebs-Henseleit (K-H) solution. (I) Carbachol (CCh), anti-ChE drugs (neostigmine, pyridostigmine, edrophonium) or DMPP (a selective ganglionic nicotinic agonist) were added to induce active contraction. (2) The effects of 4-diphenylacetoxy-N-methyl-piperidine methobromide (4-DAMP), an M3muscarinic receptor antagonist, on neostigmineor pyridostigmine-induced contraction of rat tracheal ring were examined. (3) Tetrodotoxin (TTX) was tested on the anti-ChE drugs-induced responses.PI response. The tracheal slices were incubated in K-H solution containing LiCl and3[H]myo-inositol in the presence of neostigmine or pyridostigmine with or without 4-DAMP, an M3muscarinic receptor antagonist.3[H]inositol monophosphate (IP,) formed was counted with a liquid scintillation counter.ResultsCarbachol (0.1 μM), neostigmine (1 μM), pyridostigmine (10 μM) but not edrophonium or DMPP, caused tracheal ring contraction. 4-DAMP, but not tetrodotoxin, inhibited neostigmine and pyridostigmineinduced contraction. Neostigmineor pyridostigmine-induced IP1accumulation was inhibited by 4-DAMP.ConclusionsThe data suggest that anti-ChE drugs activate the M3receptors at the tracheal effector site.