Ngatidjan D, Rand M J
J Auton Pharmacol. 1986 Dec;6(4):311-7. doi: 10.1111/j.1474-8673.1986.tb00659.x.
The effects of propranolol and of the selective beta 1- and beta 2-adrenoreceptor blocking drugs atenolol and ICI 118,551 were determined on the inhibitory responses of isolated segments of rabbit ileum to noradrenaline, isoprenaline and salbutamol and to periarterial sympathetic nerve stimulation. Responses to isoprenaline (0.04-10.24 microM) and salbutamol (1.4-89.6 microM) were blocked by propranolol in concentrations up to 5.0 and 12.8 microM, respectively. Responses to sympathetic nerve stimulation were reduced but responses to noradrenaline (0.03-1.92 microM) were unaffected by propranolol in concentrations up to 10.0 and 5.0 microM, respectively. Atenolol in concentrations up to 30.0 microM blocked responses to isoprenaline (0.04-2.56 microM) but did not affect responses to noradrenaline, salbutamol or sympathetic nerve stimulation in concentrations up to 3.0, 3.0 and 1.0 microM, respectively. However, when responses to noradrenaline and sympathetic nerve stimulation were reduced by phentolamine (1.0 microM), atenolol then produced further reductions. Responses to isoprenaline (0.04-2.56 microM) and salbutamol (1.4-89.6 microM) were blocked by ICI 118,551 in concentrations up to 0.5 microM. Responses to sympathetic nerve stimulation were reduced but responses to noradrenaline were unaffected by ICI 118,551 in concentrations up to 0.01 and 0.3 microM, respectively. Salbutamol (0.1 microM) increased the inhibitory response to sympathetic nerve stimulation and this effect was blocked by ICI 118,551 (0.01 microM). It was concluded that blockade of beta 2-adrenoreceptors, presumably located on sympathetic nerve terminals, decreases the release of transmitter noradrenaline and that blockade of beta 1-adrenoreceptors, presumably located in longitudinal smooth muscle cells, reduces the response to transmitter noradrenaline when alpha-adrenoreceptors are also blocked.
研究了普萘洛尔以及选择性β1和β2肾上腺素受体阻断药阿替洛尔和ICI 118,551对兔回肠离体节段对去甲肾上腺素、异丙肾上腺素、沙丁胺醇以及对动脉周围交感神经刺激的抑制反应的影响。对异丙肾上腺素（0.04 - 10.24微摩尔）和沙丁胺醇（1.4 - 89.6微摩尔）的反应，分别在浓度高达5.0和12.8微摩尔的普萘洛尔作用下被阻断。对交感神经刺激的反应减弱，但对去甲肾上腺素（0.03 - 1.92微摩尔）的反应，分别在浓度高达10.0和5.0微摩尔的普萘洛尔作用下不受影响。浓度高达30.0微摩尔的阿替洛尔阻断了对异丙肾上腺素（0.04 - 2.56微摩尔）的反应，但分别在浓度高达3.0、3.0和1.0微摩尔时，不影响对去甲肾上腺素、沙丁胺醇或交感神经刺激的反应。然而，当用酚妥拉明（1.0微摩尔）使对去甲肾上腺素和交感神经刺激的反应减弱时，阿替洛尔随后进一步减弱了反应。对异丙肾上腺素（0.04 - 2.56微摩尔）和沙丁胺醇（1.4 - 89.6微摩尔）的反应，在浓度高达0.5微摩尔的ICI 118,551作用下被阻断。对交感神经刺激的反应减弱，但对去甲肾上腺素的反应，分别在浓度高达0.01和0.3微摩尔的ICI 118,551作用下不受影响。沙丁胺醇（0.1微摩尔）增强了对交感神经刺激的抑制反应，且这种作用被ICI 118,551（0.01微摩尔）阻断。得出的结论是，推测位于交感神经末梢的β2肾上腺素受体的阻断减少了递质去甲肾上腺素的释放，且推测位于纵行平滑肌细胞的β1肾上腺素受体的阻断，在α肾上腺素受体也被阻断时，降低了对递质去甲肾上腺素的反应。
