The similarity in drug receptore in maxillary arterial smooth muscle of rabbit between those in anterior byssus retractor muscle of mytilus

首先，本研究探讨了兔大尾平滑肌（MASM）和贻贝前足牵开肌（ABRM）中增强药物诱导收缩受体的相似性。其次，将MASM中介导5-HT收缩反应的受体与使用5-HT1A和5-HT1B激动剂介导ABRM中5-HT松弛反应的受体进行比较。1. 5-甲氧基色胺（5-MeOT）和5-甲氧基- n， n -二甲基色胺（5-MeODMT）可增强去甲肾上腺素(NE)-和组胺（His）诱导的MASM收缩和ach诱导的ABRM收缩，但1-（3-氯苯基）哌嗪（mCPP）、8-羟基-二丙基胺四嗪（8-OH-DPAT）、间三氟甲基哌嗪（TEMPP）、对氨基苯基乙基-TEMPP （PAPP）、1-（2-甲氧基苯基）哌嗪（2MPP）和喹嗪不能增强。5-羟色胺不影响5-羟色胺和5-羟色胺对NE-、His-和ach -收缩的增强作用。更重要的是，酮丝氨酸、1-（1-萘基）哌嗪（NAP）、米安丝氨酸、环庚嘌呤和甲塞柳胺。胆囊收缩素（CCK）拮抗剂苯曲普利特和丙氨酰胺以及CCK本身、CCK-4和CCK-8都不能阻止FMRFamide对收缩的增强作用。2. 5-MeOT、5-MeODMT、8-OH-DPAT、mCPP和quipazine使MASM收缩，而TEMP P、PAPP和2MPP不使MASM收缩；5-MeOT、5-MeODMT、mCPP、8-OH-DPAT、TFMPP和PAPP使ABRM松弛，但2MPP和quipazine不使ABRM松弛。5-HT使ABRM循环AMP （cAMP）水平升高，5-MeOT、5-MeODMT、TFMPP、2MPP和quipazine使cAMP水平降低，而PAPP和mCPP对cAMP水平无影响。此外，苯特拉明和二苯胺可可逆地抑制ABRM的ache收缩，而吡唑嗪和哌替啶则不能。SCH23390可使ABRM松弛，NAP可竞争性地拮抗SCH23390诱导的松弛。从上述实验结果可以看出，两种肌肉在药理性质上存在一定的相似性，即药物诱导的收缩均由吲哚5-HT_<1a>激动剂和FMRFamide增强，MASM和ABRM中的5-HT受体均以5-HT1a亚型为主。然而，5-HT1a和5-HT1b激动剂诱导的ABRM中cAMP水平的变化与激动剂诱导的松弛无关。此外，有可能在ABRM中存在5-HT-_2样受体。在ABRM中，苯特拉明和二苯拉明不与乙酰胆碱受体形成共价键。少

Firstly, the present study was to investigate the similarity in the receptors potentiating the druginduced contraction in the maxi-lary aterail smooth muscle of rabbir (MASM) and those in the anterior byssus retractor muscle of Mytilus (ABRM). Secondly, the receptors mediating the contractile response to serotomin (5-HT) in the MASM were compared those mediating the relaxant response to 5-HT in the ABRM using some 5-HT1A and 5-HT1B agonists. 1. The norepinephrine (NE)- and histamine (His) induced contractions in the MASM and ACh-induced contraction in the ABRM were potentiated by 5methoxytryptamine (5-MeOT) and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT), but not by 1-(3-cholorophenyl) piperazien (mCPP), 8-hydroxy-dipropylaminotetraline (8-OH-DPAT), m-trifluromethylpiperazxine (TEMPP), p-aminophenylethyl-TEMPP (PAPP), 1-(2-methoxyphenyl)piperazien (2MPP) and quipazine. The potentiating actions of NE-, His- and ACh-contractions by 5-MeOT and 5-MeODMT were not prevented by 5-HT antragoni … More sts, ketanserine, 1-(1-naphthyl)piperazine (NAP), mianserine, cyproheptadine and methysergide. The potentiating actions of the contracions by FMRFamide were not prevented by cholecystokinin (CCK) antagonists, benzotript and proglumide, and also by CCK itseld, CCK-4 and CCK-8. 2. The MASM was contracted by 5-MeOT, 5-MeODMT, 8-OH-DPAT, mCPP and quipazine, but not by TEMP P, PAPP and 2MPP, wihle the ABRM was relaxed by 5-MeOT, 5-MeODMT, mCPP, 8-OH-DPAT, TFMPP and PAPP, but not by 2MPP and quipazine. Furthermore, the cyclie AMP (cAMP) levels in the ABRM were elevated by 5-HT, and decreased by 5-MeOT, 5-MeODMT, TFMPP, 2MPP and quipazine, but were not chaged by PAPP and mCPP. Additionally, The ACh-contraction in the ABRM was reversibly inhibited by benextramine and dibenamine, but not by prazocine and yohinbine. The ABRM was relaxed by SCH23390 and the SCH23390-induced relaxation was antagonized by NAP competitibely.From the above experimental results, there are some similatities between both the muscles in their pharmacological properties, that is to say, the drug-induced contractions are potenited by the indole 5-HT_<1a> agonists and FMRFamide, and 5-HT receptors in both MASM and ABRM are predominantly 5-HT1a subtype. However, the changes in cAMP levels in the ABRM induced by 5-HT1a and 5-HT1b agonists do not seen to be linked to the relaxation induced by the agonists. Moreover, There is possibility that 5-HT-_2like receptors are present in the ABRM. Benextramine and dibenamine do not form the covalent sttacvhment to the ACh receptors in the ABRM. Less