Allen J M, McHale N G, Rooney B M
Am J Physiol. 1983 Apr;244(4):H479-86. doi: 10.1152/ajpheart.1983.244.4.H479.
Norepinephrine increases the spontaneous contraction frequency of isolated bovine lymphatic vessels but, paradoxically, reduces contraction force. In this investigation contractions were elicited by electrical stimulation, applied as field stimulation or across a sucrose gap. Evoked contractions were not reduced in force by concentrations of norepinephrine that have previously been shown to dramatically reduce contractility in spontaneously active vessels. However, at higher concentrations a beta-inhibitory component of the norepinephrine effect was often observed. Simultaneous recordings of electrical and mechanical activity from spontaneously active vessels showed that each spontaneous contraction was initiated by a single action potential. Norepinephrine significantly disrupted electrical activity causing increased action potential frequency, reduction in action potential amplitude, and frequent failure of full action potential development. We conclude that norepinephrine depresses the force of spontaneous contractions by disruption of spontaneous pacemaking rather than by any direct effect on vessel contractility.
去甲肾上腺素可增加离体牛淋巴管的自发收缩频率，但矛盾的是，它会降低收缩力。在本研究中，通过电场刺激或跨蔗糖间隙施加电刺激来引发收缩。先前已表明能显著降低自发活动血管收缩性的去甲肾上腺素浓度，并不会降低诱发收缩的力量。然而，在更高浓度时，经常会观察到去甲肾上腺素作用的β抑制成分。对自发活动血管的电活动和机械活动进行同步记录显示，每次自发收缩均由单个动作电位引发。去甲肾上腺素显著扰乱电活动，导致动作电位频率增加、动作电位幅度减小以及频繁出现完全动作电位发育失败的情况。我们得出结论，去甲肾上腺素通过破坏自发起搏而非对血管收缩性的任何直接作用来抑制自发收缩的力量。
