Karashima T, Kuriyama H
Br J Pharmacol. 1981 Oct;74(2):495-504. doi: 10.1111/j.1476-5381.1981.tb09996.x.
1 The membrane properties of smooth muscle cells and neuromuscular transmission in the guinea-pig basilar artery were investigated by use of microelectrodes.2 The membrane potential was -47.0 mV and the muscle tissue possessed cable-like properties as determined by the current-voltage relationships. The mean value of the spacè constant was 0.78 mm.3 An outward current produced a graded response and, in some cases, spike generation. This membrane response was enhanced in the presence of tetraethylammonium (TEA, 5 mM), and an increased concentration of TEA (10 mM) generated spontaneous spikes in most of the cells. Action potentials induced by TEA were abolished in the presence of MnCl(2) (5 mM) but not by isoprenaline (4 x 10(-6) M).4 Acetylcholine (ACh), over 10(-7) M, hyperpolarized the membrane and decreased the membrane resistance. This hyperpolarization increased in the presence of low K (below 5.9 mM), but decreased in K concentrations over 17.8 mM. Pretreatment with atropine (10(-6) M) suppressed the ACh-induced hyperpolarization. Therefore, this action of ACh is due to an increase in the K-conductance of the membrane produced by activation of the muscarinic receptors.5 Noradrenaline in concentrations up to 10(-4) M did not modify the membrane potential and resistance, while 10(-5) M, histamine, 5-hydroxytryptamine and adenosine triphosphate (ATP) depolarized the membrane. The depolarization induced by histamine or ATP was suppressed by reducing Na. The histamine-induced depolarization was accompanied by an increase and the ATP-induced one by a decrease in the membrane resistance. The action of histamine was suppressed by treatment with H(1)- but not H(2)-receptor blocking agents (dephenhydramine and cimetidine, respectively).6 Perivascular nerve stimulation (0.2 ms pulse duration) evoked excitatory junction potentials (e.j.ps). An increase in the number and frequency of stimuli enhanced the e.j.p. amplitude. In the presence of 1 mM TEA, a spike was evoked on the e.j.ps. A very high concentration of phentolamine (3.6 x 10(-4) M) or the usual concentration of tetrodotoxin (10(-7) M) abolished the generation of e.j.ps. Spontaneously generated miniature e.j.ps were never recorded from the resting membrane.7 The results are discussed in relation to regional specificities of smooth muscle cells of cerebral arteries in the guinea-pig.
运用微电极对豚鼠基底动脉平滑肌细胞的膜特性及神经肌肉传递进行了研究。
膜电位为 -47.0 mV,通过电流 - 电压关系测定,肌肉组织具有电缆样特性。空间常数的平均值为0.78 mm。
外向电流产生分级反应,在某些情况下还会产生峰电位。在四乙铵(TEA,5 mM)存在时,这种膜反应增强,而TEA浓度增加(10 mM)时,大多数细胞会产生自发峰电位。TEA诱导的动作电位在MnCl₂(5 mM)存在时被消除,但在异丙肾上腺素(4×10⁻⁶ M)存在时未被消除。
乙酰胆碱(ACh)浓度超过10⁻⁷ M时,使膜超极化并降低膜电阻。在低[K]ₒ(低于5.9 mM)存在时,这种超极化增强,但在[K]ₒ浓度超过17.8 mM时降低。用阿托品(10⁻⁶ M)预处理可抑制ACh诱导的超极化。因此,ACh的这种作用是由于毒蕈碱受体激活导致膜K⁺电导增加。
浓度高达10⁻⁴ M的去甲肾上腺素未改变膜电位和电阻,而10⁻⁵ M的组胺、5 - 羟色胺和三磷酸腺苷(ATP)使膜去极化。降低[Na]ₒ可抑制组胺或ATP诱导的去极化。组胺诱导的去极化伴随着膜电阻增加,而ATP诱导的去极化伴随着膜电阻降低。组胺的作用可被H₁受体阻断剂(分别为苯海拉明)而非H₂受体阻断剂(西咪替丁)处理所抑制。
血管周围神经刺激(脉冲持续时间0.2 ms)诱发兴奋性接头电位(e.j.ps)。刺激数量和频率增加会增强e.j.p.幅度。在1 mM TEA存在时,e.j.ps上会诱发峰电位。非常高浓度的酚妥拉明(3.6×10⁻⁴ M)或常用浓度的河豚毒素(10⁻⁷ M)可消除e.j.ps的产生。从未在静息膜上记录到自发产生的微小e.j.ps。
结合豚鼠脑动脉平滑肌细胞的区域特异性对结果进行了讨论。