Zelcer E, Sperelakis N
Pflugers Arch. 1981 Nov;392(1):72-8. doi: 10.1007/BF00584585.
The regulation of blood vessel diameter is under the control of the autonomic nervous system (as well as hormones and metabolites), sympathetic nerve stimulation evoking depolarizing post-synaptic potentials. Excitatory junction potentials (EJPs) were recorded from vascular smooth muscle cells of guinea-pig small mesenteric arteries (pressurized) following nerve stimulation. Repetitive stimulation (greater than 5Hz) led to summation of EJPs, which evoked spikes and vasoconstriction. Replacing extracellular Na+ with choline (plus atropine) resulted in a decrease in EJP amplitude, but spike amplitude and maximum rate of rise (+Vmax) were unaffected. Decreasing the Ca2+ concentration produced decreases in EJP amplitude and spike +Vmax. Verapamil and bepridil, agents that depress Ca2+ influx in vascular and visceral smooth muscle, depolarized the membrane and depressed EJPs and spikes at higher concentrations (10(-5) M and 5 X 10(-6) M, respectively). The data indicate that EJPs are dependent on external Na+ and Ca2+ ions, and that spikes are dependent on Ca2+. Thus, neuromuscular transmission in this muscle is similar to that in non-vascular smooth muscles, such as intestinal muscles and vas deferens.
血管直径的调节受自主神经系统（以及激素和代谢产物）的控制，交感神经刺激可引发去极化的突触后电位。在神经刺激后，从豚鼠小肠系膜动脉（处于压力状态）的血管平滑肌细胞记录兴奋性接头电位（EJP）。重复刺激（大于5Hz）导致EJP的总和，进而引发动作电位和血管收缩。用胆碱（加阿托品）替代细胞外Na+会导致EJP幅度降低，但动作电位幅度和最大上升速率（+Vmax）不受影响。降低Ca2+浓度会导致EJP幅度和动作电位+Vmax降低。维拉帕米和苄普地尔是抑制血管和内脏平滑肌中Ca2+内流的药物，在较高浓度（分别为10^(-5)M和5×10^(-6)M）时会使膜去极化并抑制EJP和动作电位。数据表明，EJP依赖于细胞外Na+和Ca2+离子，而动作电位依赖于Ca2+。因此，该肌肉中的神经肌肉传递与非血管平滑肌（如肠道肌肉和输精管）中的相似。
