Seiler Roland, Rickenbacher Andreas, Shaw Sidney, Haefliger Simon, Balsiger Bruno M
Gastroenterology Unit (Prof. U. Scheurer), University Hospital Bern, University of Bern, Bern, Switzerland.
J Gastrointest Surg. 2008 Jun;12(6):1087-93. doi: 10.1007/s11605-007-0327-4. Epub 2007 Sep 19.
Gut motility is modulated by adrenergic mechanisms. The aim of our study was to examine mechanisms of selective adrenergic receptors in rat jejunum. Spontaneous contractile activity of longitudinal muscle strips from rat jejunum was measured in 5-ml tissue chambers. Dose-responses (six doses, 10(-7) -3 x 10(-5)M) to norepinephrine (NE, nonspecific), phenylephrine (PH, alpha1), clonidine (C, alpha2), prenalterol (PR, beta1), ritodrine (RI, beta2), and ZD7714 (ZD, beta3) were evaluated with and without tetrodotoxin (TTX, nerve blocker). NE(3 x 10(-5)M) inhibited 74 +/- 5% (mean +/- SEM) of spontaneous activity. This was the maximum effect. The same dose of RI(beta2), PH(alpha1), or ZD(beta(3)) resulted in an inhibition of only 56 +/- 5, 43 +/- 4, 33 +/- 6, respectively. The calculated concentration to induce 50% inhibition (EC50) of ZD(beta3) was similar to NE, whereas higher concentrations of PH(alpha1) or RI(beta2) were required. C(alpha2) and PR(beta1) had no effect. TTX changed exclusively the EC50 of RI from 4.4 +/- 0.2 to 2.7 +/- 0.8% (p < 0.04). Contractility was inhibited by NE (nonspecific). PH(alpha1), RI(beta2), and ZD(beta3) mimic the effect of NE. TTX reduced the inhibition by RI. Our results suggest that muscular alpha1, beta2, and beta3 receptor mechanisms mediate adrenergic inhibition of contractility in rat jejunum. beta2 mechanisms seem to involve also neural pathways.
肠道运动受肾上腺素能机制调节。我们研究的目的是探讨大鼠空肠中选择性肾上腺素能受体的机制。在5毫升组织浴槽中测量大鼠空肠纵行肌条的自发收缩活动。评估了去甲肾上腺素（NE，非特异性）、苯肾上腺素（PH，α1）、可乐定（C，α2）、普瑞特罗（PR，β1）、利托君（RI，β2）和ZD7714（ZD，β3）在有和没有河豚毒素（TTX，神经阻滞剂）情况下的剂量反应（六种剂量，10^(-7)-3×10^(-5)M）。NE（3×10^(-5)M）抑制了74±5%（平均值±标准误）的自发活动。这是最大效应。相同剂量的RI（β2）、PH（α1）或ZD（β3）分别仅导致56±5%、43±4%、33±6%的抑制。诱导ZD（β3）50%抑制（EC50）的计算浓度与NE相似，而需要更高浓度的PH（α1）或RI（β2）。C（α2）和PR（β1）没有作用。TTX仅将RI的EC50从4.4±0.2变为2.7±0.8%（p<0.04）。收缩性被NE（非特异性）抑制。PH（α1）、RI（β2）和ZD（β3）模拟了NE的作用。TTX降低了RI的抑制作用。我们的结果表明，肌肉α1、β2和β3受体机制介导了大鼠空肠中肾上腺素能对收缩性的抑制。β2机制似乎也涉及神经通路。
