Byrne N G, Muir T C
Br J Pharmacol. 1985 May;85(1):149-61. doi: 10.1111/j.1476-5381.1985.tb08842.x.
The response of the bovine retractor penis (BRP) to stimulation of non-adrenergic, non-cholinergic (NANC) inhibitory nerves and to an inhibitory extract prepared from this muscle have been studied using intracellular microelectrode, sucrose gap and conventional mechanical recording techniques. Both inhibitory nerve stimulation and inhibitory extract hyperpolarized the membrane potential and relaxed spontaneous or guanethidine (3 X 10(-5) M)-induced tone. These effects were accompanied by an increase in membrane resistance. Following membrane potential displacement from an average value of -53 +/- 7 mV (n = 184; Byrne & Muir, 1984) inhibitory potentials to nerve stimulation were abolished at approximately -30 mV; there was no evidence of reversal. Displacement by inward hyperpolarizing current over the range -45 to -60 mV increased the inhibitory response to nerve stimulation and to inhibitory extract; at more negative potential values (above approximately -60 mV) the inhibitory potential decreased and was abolished (approximately -103 mV). There was no evidence of reversal. Removal of [K+]o reversibly reduced hyperpolarization to nerve stimulation and inhibitory extract. No enhancement was observed. Increasing the [K+]o to 20 mM reduced the inhibitory potential to nerve stimulation but this was restored by passive membrane hyperpolarization. Inhibitory potentials were obtained at membrane potential values exceeding that of the estimated EK (-49 mV). [Cl-]o-free or [Cl-]o-deficient solutions reduced and abolished (after some 20-25 min) the hyperpolarization produced by inhibitory nerve stimulation or inhibitory extract. The inhibitory potential amplitude following nerve stimulation was not restored by passive displacement of the membrane potential from -26 to -104 mV approximately. Ouabain (1-5 X 10(-5) M) reduced then (45-60 min later) abolished the inhibitory potential to nerve stimulation. The effects of this drug on the extract were not investigated. It is concluded that the inhibitory response to nerve stimulation and extract in the BRP may involve several ionic species. However, unlike that in gastrointestinal muscles the NANC response in the BRP is accompanied by an increased membrane resistance and does not primarily involve K+. The underlying mechanisms for the inhibitory response to both NANC nerve stimulation and inhibitory extract appear to be similar, compatible with the view that the latter may contain the inhibitory transmitter released from these nerves in this tissue.
利用细胞内微电极、蔗糖间隙和传统机械记录技术，研究了牛阴茎退缩肌（BRP）对非肾上腺素能、非胆碱能（NANC）抑制性神经刺激以及对从该肌肉制备的抑制性提取物的反应。抑制性神经刺激和抑制性提取物均使膜电位超极化，并使自发或胍乙啶（3×10⁻⁵M）诱导的张力松弛。这些效应伴随着膜电阻的增加。当膜电位从-53±7mV（n = 184；Byrne和Muir，1984）的平均值发生位移后，神经刺激的抑制性电位在约-30mV时消失；没有反转的迹象。通过内向超极化电流在-45至-60mV范围内进行位移，增加了对神经刺激和抑制性提取物的抑制反应；在更负的电位值（约-60mV以上）时，抑制性电位降低并消失（约-103mV）。没有反转的迹象。去除细胞外[K⁺]可逆地减少了对神经刺激和抑制性提取物的超极化。未观察到增强作用。将细胞外[K⁺]增加到20mM可降低对神经刺激的抑制性电位，但通过被动膜超极化可使其恢复。在膜电位值超过估计的钾平衡电位（EK，-49mV）时可获得抑制性电位。无氯或低氯溶液可降低并（约20 - 25分钟后）消除抑制性神经刺激或抑制性提取物产生的超极化。通过将膜电位从约-26mV被动位移到-104mV，不能恢复神经刺激后的抑制性电位幅度。哇巴因（1 - 5×10⁻⁵M）先降低然后（45 - 60分钟后）消除对神经刺激的抑制性电位。未研究该药物对提取物的影响。得出的结论是，BRP对神经刺激和提取物的抑制反应可能涉及多种离子。然而，与胃肠道肌肉不同，BRP中的NANC反应伴随着膜电阻增加，且主要不涉及钾离子。对NANC神经刺激和抑制性提取物的抑制反应的潜在机制似乎相似，这与后者可能含有从该组织中的这些神经释放的抑制性递质的观点一致。
