Carpenter F G
Am J Physiol. 1985 Oct;249(4 Pt 2):R417-23. doi: 10.1152/ajpregu.1985.249.4.R417.
The potentiation of nerve-induced bladder contractions (NIC) by tetraethylammonium chloride (TEA), K+, or carbachol could result from a greater Ca2+ entry through Ca2+ channels in the muscle or from a greater release of transmitter by nerve terminals. Contractions of equal magnitude by the rat urinary bladder in vitro were initiated by carbachol, K+, or transmural stimulation of urinary bladder motor nerves at 1 Hz. Contractions elicited by K+ or carbachol were drastically reduced by verapamil (0.5 microM), but NICs were unaffected. Thus the role of Ca2+ channels in NICs seems uncertain. NICs are potentiated approximately 50% by K+ (15 mM), carbachol (0.5 microM), or 4-aminopyridine (0.2 mM) and over twofold by TEA (5 mM). Although verapamil (1-5 microM) reduced NICs in a dose-dependent relation, potentiation by each compound was the same. Thus Ca2+ channels probably play no role in potentiation. The resistance of the bladder to distention reflects its viscoelasticity and is Ca2+ sensitive. Because viscoelasticity was decreased by verapamil coincident with the reduction in NICs, both may result from lowered intracellular Ca2+ (Cai2+). However, because the potentiating compounds failed to restore bladder viscoelasticity, they probably did not elevate Cai2+. Therefore, in verapamil-treated preparations potentiation is most probably caused by an enhancement of transmitter release.
氯化四乙铵（TEA）、钾离子（K⁺）或卡巴胆碱对神经诱导的膀胱收缩（NIC）的增强作用，可能是由于更多的钙离子通过肌肉中的钙离子通道进入，或者是由于神经末梢释放了更多的递质。在体外，用卡巴胆碱、K⁺或1Hz经壁刺激膀胱运动神经引发大鼠膀胱产生等强度的收缩。维拉帕米（0.5微摩尔）可显著降低由K⁺或卡巴胆碱引起的收缩，但对NIC无影响。因此，钙离子通道在NIC中的作用似乎并不确定。K⁺（15毫摩尔）、卡巴胆碱（0.5微摩尔）或4-氨基吡啶（0.2毫摩尔）可使NIC增强约50%，而TEA（5毫摩尔）可使其增强两倍以上。尽管维拉帕米（1 - 5微摩尔）以剂量依赖的方式降低了NIC，但每种化合物的增强作用相同。因此，钙离子通道可能在增强作用中不起作用。膀胱对扩张的抵抗力反映了其粘弹性，且对钙离子敏感。由于维拉帕米降低粘弹性的同时也降低了NIC，二者可能都是细胞内钙离子（Cai²⁺）浓度降低所致。然而，由于增强性化合物未能恢复膀胱粘弹性，它们可能并未升高Cai²⁺。因此，在维拉帕米处理的标本中，增强作用很可能是由递质释放增强引起的。
