Suzuki T
Nihon Heikatsukin Gakkai Zasshi. 1983 Apr;19(2):123-38.
Many workers have reported that alpha-adrenergic drugs activate and beta-adrenergic drugs suppress the ureteral activity. On the other hand, recent studies have proved that the pacemaker in the renal pelvis controls the ureteral peristalsis. In this study, in vivo and in vitro experiments were performed to explore the effects of autonomic drugs on pelvic pacemaker controlling the ureteral peristalsis. It was suggested that both of noradrenaline and isoproterenol stimulated the pacemaker activity itself, the former, however, elevated the renal pelvic pressure to accelerate the propagation of pacemaker activity consequently, while the latter decreased the renal pelvic pressure to suppress the propagation consequently. Acetylcholine stimulated the pacemaker activity and its propagation transiently, but base line of renal pelvic pressure with increased contraction pressure was decreased after drug administration. Furthermore, acetylcholine sometimes developed the retrograde peristaltic contraction from ureter to pacemaker region though the pelviureteral junction. Then acetylcholine might affect directly on ureter rather than on pacemaker itself and its propagation.
许多工作人员报告称，α-肾上腺素能药物会激活输尿管活动，而β-肾上腺素能药物会抑制输尿管活动。另一方面，最近的研究证明肾盂中的起搏器控制着输尿管蠕动。在本研究中，进行了体内和体外实验，以探究自主神经药物对控制输尿管蠕动的肾盂起搏器的影响。结果表明，去甲肾上腺素和异丙肾上腺素均刺激起搏器活动本身，然而，前者会升高肾盂压力，从而加速起搏器活动的传播，而后者会降低肾盂压力，从而抑制传播。乙酰胆碱短暂刺激起搏器活动及其传播，但给药后肾盂压力基线随收缩压升高而降低。此外，乙酰胆碱有时会通过肾盂输尿管连接部产生从输尿管到起搏器区域的逆行蠕动收缩。因此，乙酰胆碱可能直接作用于输尿管，而非起搏器本身及其传播。
