可乐定对体外大鼠逼尿肌条电诱导收缩的影响。
The effects of clonidine on electrically-induced contractions of rat detrusor strips in vitro.
作者信息
Santicioli P, Maggi C A, Meli A
出版信息
J Auton Pharmacol. 1983 Sep;3(3):161-6. doi: 10.1111/j.1474-8673.1983.tb00531.x.
Clonidine (10(-9)-3 X 10(-6) M) produced a concentration dependent inhibition of field stimulation-induced contractions of rat detrusor muscle strip at 0.1 and 1 Hz which were completely abolished by tetrodotoxin (5 X 10(-7) M) but were unaffected by hexamethonium (10(-5) M). Pretreatment with yohimbine (10(-8)-10(-7) M) did not modify the amplitude of contractions but produced a rightward parallel shift of clonidine's cumulative response curve without a depression of the maximal response. The corresponding pA2 value for yohimbine was 8.44 +/- 0.1. Atropine (3 X 10(-6) M) produced a partial inhibition of contractions at both frequencies. In the presence of atropine the cumulative response curve of clonidine was significantly reduced at 1 but not at 0.1 Hz. Indomethacin (5 X 10(-5) M) and theophylline (2 X 10(-4) M) produced a partial inhibition of amplitude of contractions at both frequencies without any interference with the effect of a supramaximal concentration of clonidine. Prazosin (10(-6) M), propranolol (10(-6) M), chlorpheniramine (10(-6) M), ranitidine (10(-6) M), haloperidol (10(-7) M), pizotifen (10(-6) M), naloxone (10(-6) M), quinidine (10(-6) M), strychnine (10(-5) M) or picrotoxin (10(-5) M) neither affected the amplitude of contractions at either frequency nor antagonized clonidine effects. The contractile response of non stimulated strips to acetylcholine (10(-5) M), carbachol (3 X 10(-6) M) and ATP (10(-3) M) were not significantly influenced by pretreatment with clonidine (3 X 10(-6) M). These results suggest that stimulation of prejunctional alpha 2-adrenoreceptors located on postganglionic nerve endings might reduce the output of excitatory neurotransmitter(s) in rat urinary bladder.
可乐定（10⁻⁹ - 3×10⁻⁶ M）对大鼠逼尿肌条在0.1 Hz和1 Hz频率下由场刺激诱导的收缩产生浓度依赖性抑制，这种抑制被河豚毒素（5×10⁻⁷ M）完全消除，但不受六甲铵（10⁻⁵ M）影响。用育亨宾（10⁻⁸ - 10⁻⁷ M）预处理不改变收缩幅度，但使可乐定的累积反应曲线向右平行移动，且最大反应无降低。育亨宾相应的pA₂值为8.44±0.1。阿托品（3×10⁻⁶ M）在两个频率下均产生部分收缩抑制。在阿托品存在下，可乐定的累积反应曲线在1 Hz时显著降低，但在0.1 Hz时未降低。吲哚美辛（5×10⁻⁵ M）和茶碱（2×10⁻⁴ M）在两个频率下均产生部分收缩幅度抑制，且不干扰可乐定超最大浓度的作用。哌唑嗪（10⁻⁶ M）、普萘洛尔（10⁻⁶ M）、氯苯那敏（10⁻⁶ M）、雷尼替丁（10⁻⁶ M）、氟哌啶醇（10⁻⁷ M）、苯噻啶（10⁻⁶ M）、纳洛酮（10⁻⁶ M）、奎尼丁（10⁻⁶ M）、士的宁（10⁻⁵ M）或印防己毒素（10⁻⁵ M）既不影响任一频率下的收缩幅度，也不拮抗可乐定的作用。用可乐定（3×10⁻⁶ M）预处理对未刺激条带对乙酰胆碱（10⁻⁵ M）、卡巴胆碱（3×10⁻⁶ M）和ATP（10⁻³ M）的收缩反应无显著影响。这些结果表明，刺激位于节后神经末梢的节前α₂ - 肾上腺素能受体可能会减少大鼠膀胱中兴奋性神经递质的释放。
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