Ito Y, Tajima K
Br J Pharmacol. 1982 Mar;75(3):433-40. doi: 10.1111/j.1476-5381.1982.tb09158.x.
1 Effects of noradrenaline or isoprenaline on the membrane and contractile properties of the smooth muscle cell, or on the excitatory neuro-effector transmission in the dog trachea, in vitro, were observed by use of microelectrodes and double sucrose gap methods.2 Noradrenaline (<5 x 10(-6) M) or isoprenaline (<5 x 10(-7) M) modified neither the membrane potential nor the membrane resistance. Increased concentrations of noradrenaline (>5 x 10(-5) M) depolarized and isoprenaline (>5 x 10(-7) M) hyperpolarized the membrane, and these actions were suppressed by phentolamine and propranolol respectively. Both catecholamines reduced the membrane resistance.3 Noradrenaline (5 x 10(-6) M) or isoprenaline (5 x 10(-7) M) reduced the resting tension, raised the mechanical threshold required to produce the contraction and suppressed the amplitude of phasic contractions evoked by electrical depolarization of the membrane.4 The action potential evoked by an outward current pulse in the presence of tetraethylammonium (TEA) was not affected by 5 x 10(-6) M isoprenaline, while the mechanical response was markedly suppressed.5 The excitatory junction potential (e.j.p.) evoked by electrical field stimulation was blocked by atropine. Noradrenaline (5 x 10(-7) M) or isoprenaline (5 x 10(-8) M) suppressed the amplitude of e.j.p. with no change in the membrane potential or input membrane resistance. Depression in the amplitude of e.j.ps produced by noradrenaline or isoprenaline reduced the amplitude of phasic contractions evoked by e.j.ps.6 These inhibitory actions of the catecholamines on mechanical responses and on e.j.ps were suppressed by pretreatment with propranolol (4 x 10(-6) M).7 Dog tracheal smooth muscles are innervated by cholinergic excitatory and adrenergic inhibitory systems. Electrical field stimulation produced excitation of both cholinergic and adrenergic nerve fibres, and propranolol (4 x 10(-6) M) enhanced the amplitude of e.j.p. generated by excitation of cholinergic nerves when repetitive stimulation (10 stimuli at 20 Hz) was used, but not the amplitude of the e.j.p. evoked by a single stimulus.8 5-Hydroxytryptamine (6 x 10(-6) M) produced a tonic contracture of the dog trachea. After pretreatment with atropine (4 x 10(-6) M), field stimulation (50 mus in duration and repetitive stimuli at 20 Hz) induced reversal of the contracture induced by 5-hydroxytryptamine and this was abolished by propranolol (5 x 10(-6) M).9 These results indicate that endogenous or exogenous catecholamines, in relatively low concentrations, predominantly activate beta-adrenoceptors in the pre- and post-junctional membrane in the dog trachea, and induce muscle relaxation.
运用微电极和双蔗糖间隙法，在体外观察了去甲肾上腺素或异丙肾上腺素对犬气管平滑肌细胞膜及收缩特性，或对兴奋性神经 - 效应器传递的影响。
去甲肾上腺素（<5×10⁻⁶ M）或异丙肾上腺素（<5×10⁻⁷ M）既不改变膜电位也不改变膜电阻。去甲肾上腺素浓度增加（>5×10⁻⁵ M）使膜去极化，异丙肾上腺素浓度增加（>5×10⁻⁷ M）使膜超极化，且这些作用分别被酚妥拉明和普萘洛尔抑制。两种儿茶酚胺均降低膜电阻。
去甲肾上腺素（5×10⁻⁶ M）或异丙肾上腺素（5×10⁻⁷ M）降低静息张力，提高产生收缩所需的机械阈值，并抑制膜电去极化诱发的相性收缩幅度。
在四乙铵（TEA）存在下，外向电流脉冲诱发的动作电位不受5×10⁻⁶ M异丙肾上腺素影响，而机械反应则明显受到抑制。
电场刺激诱发的兴奋性接头电位（e.j.p.）被阿托品阻断。去甲肾上腺素（5×10⁻⁷ M）或异丙肾上腺素（5×10⁻⁸ M）抑制e.j.p.的幅度，而膜电位或输入膜电阻无变化。去甲肾上腺素或异丙肾上腺素引起的e.j.p.幅度降低减少了由e.j.p.诱发的相性收缩幅度。
普萘洛尔（=4×10⁻⁶ M）预处理可抑制儿茶酚胺对机械反应和e.j.p.的这些抑制作用。
犬气管平滑肌受胆碱能兴奋性和肾上腺素能抑制性系统支配。电场刺激可兴奋胆碱能和肾上腺素能神经纤维，当采用重复刺激（20 Hz下10次刺激）时，普萘洛尔（4×10⁻⁶ M）可增强胆碱能神经兴奋产生的e.j.p.幅度，但对单个刺激诱发的e.j.p.幅度无增强作用。
5 - 羟色胺（6×10⁻⁶ M）引起犬气管强直性收缩。用阿托品（4×10⁻⁶ M）预处理后，电场刺激（持续50 μs，20 Hz重复刺激）可使5 - 羟色胺诱发的收缩逆转，且这一作用被普萘洛尔（5×10⁻⁶ M）消除。
这些结果表明，内源性或外源性儿茶酚胺在相对低浓度时，主要激活犬气管节前和节后膜上的β - 肾上腺素能受体，并诱导肌肉松弛。
