Belfrage E
Acta Physiol Scand. 1978 Apr;102(4):459-68. doi: 10.1111/j.1748-1716.1978.tb06094.x.
The present experiments were undertaken to study the balance between vascular alpha- and beta-adrenoceptors in canine subcutaneous adipose tissue during sympathetic nerve stimulation and noradrenaline injections. Propranolol potentiated and prolonged the vasoconstrictor response to close i.a. injections of noradrenaline. The vasoconstriction induced by brief nerve stimulation (0.5 to 8 Hz) was, however, unaltered by the beta-adrenoceptor blockade. During prolonged nerve stimulation the vasoconstrictor response was well maintained at 1.5 Hz but at 4 Hz there was a gradual escape. The escape phenomenon at 4 Hz was diminished by propranolol. The beta1-selective antagonist practolol, like propranolol, potentiated and prolonged the vasoconstriction induced by noradrenaline injections and reduced the vasoconstrictor escape during prolonged nerve stimulation at 4 Hz. Furthermore, the vasodilatation induced by noradrenaline injection or nerve stimulation during alpha-adrenoceptor blockade was diminished by practolol. Practolol also blocked the lipolytic response to noradrenaline and nerve stimulation. The beta2-selective antagonist H35/25 blocked the effects of the beta2-selective agonist salbutamol but failed to alter noradrenaline as well as nerve stimulation induced vascular and lipolytic beta-adrenoceptor responses. The present results provide further support for the hypothesis that vascular beta-adrenoceptors in adipose tissue are humoral (noninnervated), preferentially activated by circulating noradrenaline. Moreover, both vascular and lipolytic beta-adrenoceptors activated by noradrenaline in adipose tissue are best classified as beta1-adrenoceptors.
本实验旨在研究犬皮下脂肪组织在交感神经刺激和去甲肾上腺素注射过程中血管α-和β-肾上腺素能受体之间的平衡。普萘洛尔增强并延长了对近距离动脉内注射去甲肾上腺素的血管收缩反应。然而，短暂神经刺激（0.5至8赫兹）引起的血管收缩不受β-肾上腺素能受体阻断的影响。在长时间神经刺激期间，1.5赫兹时血管收缩反应得到良好维持，但在4赫兹时出现逐渐逃逸现象。普萘洛尔可减轻4赫兹时的逃逸现象。β1选择性拮抗剂普拉洛尔与普萘洛尔一样，增强并延长了去甲肾上腺素注射引起的血管收缩，并减少了4赫兹长时间神经刺激期间的血管收缩逃逸。此外，普拉洛尔可减轻α-肾上腺素能受体阻断期间去甲肾上腺素注射或神经刺激引起的血管舒张。普拉洛尔还阻断了对去甲肾上腺素和神经刺激的脂解反应。β2选择性拮抗剂H35/25阻断了β2选择性激动剂沙丁胺醇的作用，但未能改变去甲肾上腺素以及神经刺激诱导的血管和脂解β-肾上腺素能受体反应。目前的结果为脂肪组织中血管β-肾上腺素能受体是体液性（非神经支配）、优先被循环去甲肾上腺素激活这一假说提供了进一步支持。此外，脂肪组织中由去甲肾上腺素激活的血管和脂解β-肾上腺素能受体最好归类为β1-肾上腺素能受体。
