Dahlöf C, Kahan T, Ablad B
Acta Physiol Scand. 1987 Apr;129(4):499-503. doi: 10.1111/j.1748-1716.1987.tb08089.x.
Prejunctional beta-adrenoceptor-mediated modulation of endogenous noradrenaline (NA) overflow elicited by sympathetic nerve stimulation was studied in blood-perfused canine gracilis muscle in situ. An attempt was made to subclassify these beta-adrenoceptors by comparing the effects of beta 1-selective (metoprolol) and non-selective (propranolol) beta-adrenoceptor blockade. Animals were pre-treated with desipramine and phenoxybenzamine in order to counteract possible influences of neuronal uptake and stimulation-evoked changes in vascular resistance on the diffusion of NA into the blood stream. Metoprolol did not decrease stimulation-evoked NA overflow, as compared with control experiments (-10 and -8%, respectively). However, propranolol reduced stimulation-evoked NA overflow by 30% in metoprolol pre-treated animals (P less than 0.05 vs. control experiments). Both antagonists elevated basal perfusion pressure, suggesting that vascular post-junctional beta 1- as well as beta 2-adrenoceptors are present. Propranolol increased stimulation-evoked vasoconstriction in metoprolol pre-treated animals, indicating that neuronally released NA may activate postjunctional beta 2-adrenoceptors under these experimental conditions. In conclusion, our findings suggest that NA release can be enhanced by activation of prejunctional beta 2-adrenoceptors in vivo.
在原位血液灌注的犬股薄肌中，研究了接头前β-肾上腺素能受体介导的对交感神经刺激引起的内源性去甲肾上腺素（NA）溢出的调节作用。通过比较β1选择性（美托洛尔）和非选择性（普萘洛尔）β-肾上腺素能受体阻断的作用，尝试对这些β-肾上腺素能受体进行亚分类。为了抵消神经元摄取以及刺激引起的血管阻力变化对NA扩散到血流中的可能影响，动物预先用去甲丙咪嗪和酚苄明进行处理。与对照实验相比（分别为-10%和-8%），美托洛尔并未降低刺激引起的NA溢出。然而，在预先用美托洛尔处理的动物中，普萘洛尔使刺激引起的NA溢出降低了30%（与对照实验相比，P<0.05）。两种拮抗剂均升高了基础灌注压，提示存在血管后接头β1以及β2肾上腺素能受体。在预先用美托洛尔处理的动物中，普萘洛尔增加了刺激引起的血管收缩，表明在这些实验条件下，神经元释放的NA可能激活接头后β2肾上腺素能受体。总之，我们的研究结果提示，体内接头前β2肾上腺素能受体的激活可增强NA释放。
