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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Effects of imidazolines on neurogenic contraction in isolated urinary bladder detrusor strips from rabbit
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Effects of imidazolines on neurogenic contraction in isolated urinary bladder detrusor strips from rabbit

机译：咪唑啉对家兔离体膀胱逼尿肌条神经源性收缩的影响

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摘要

Moxonidine and clonidine, which are imidazoline compounds, are sympathetic modulators used as centrally acting antihypertensive drugs. Moxonidine, clonidine, and agmatine produce extensive effects in mammalian tissues via imidazoline recognition sites (or receptors) or a2-adrenoceptors. To investigate the effects of imidazolines on the function of the urinary bladder, we tested the effects of moxonidine, clonidine, and agmatine on the neurogenic contraction induced by electric field stimulation, and on the post-synaptic receptors in isolated urinary bladder detrusor strips from rabbit. Both moxonidine at 1.0-10.0 μmol/L and clonidine at 0.1-10.0 μmol/L inhibited electric-field-stimulation-induced contraction in a concentration-dependent manner, but not agmatine (10.0-1000.0 μmol/L). Both moxonidine and clonidine failed to affect carbachol or adenosine-triphosphate-induced contractions; however, 1000.0 μmol/L agmatine significantly increased these contractions. Our study indicates that (i) moxonidine and clonidine produce a concentration-dependent inhibition of the neurogenic contractile responses to electric field stimulation in isolated detrusor strips from male New Zealand rabbits; (ii) post-synaptic muscarinic receptor and purinergic receptor stimulation are not involved in the responses of moxinidine and clonidine in this study; (iii) the inhibitory effects of these agents are probably not mediated by presynaptic imidazoline receptors.
机译：作为咪唑啉化合物的莫索尼定和可乐定是用作中枢性降压药的交感调节剂。莫索尼定，可乐定和胍丁胺通过咪唑啉识别位点（或受体）或α2-肾上腺素受体在哺乳动物组织中产生广泛的作用。为了研究咪唑啉对膀胱功能的影响，我们测试了莫索尼定，可乐定和胍丁胺对电场刺激诱导的神经源性收缩的影响，以及对兔离体膀胱逼尿肌条中突触后受体的影响。 。 1.0-10.0μmol/ L的莫索尼定和0.1-10.0μmol/ L的可乐定均以浓度依赖的方式抑制电场刺激诱导的收缩，但胍丁胺（10.0-1000.0μmol/ L）却不。莫索尼定和可乐定均未影响卡巴胆碱或三磷酸腺苷引起的收缩;然而，1000.0μmol/ L胍丁胺显着增加这些收缩。我们的研究表明：（i）莫索尼定和可乐定在雄性新西兰兔离体逼尿肌条中对电场刺激的神经源性收缩反应产生浓度依赖性抑制; （ii）在这项研究中，突触后毒蕈碱受体和嘌呤能受体的刺激不参与莫西替丁和可乐定的反应; （iii）这些药物的抑制作用可能不是由突触前咪唑啉受体介导的。

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