Osswald W
Department of Pharmacology and Therapeutics, Faculty of Medicine, Porto University, Portugal.
J Neural Transm Suppl. 1991;34:157-62. doi: 10.1007/978-3-7091-9175-0_20.
Chemical or surgical sympathetic denervation of blood vessels causes marked changes of the effector cells. Since postganglionic sympathetic cotransmission by noradrenaline and adenosine 5'-triphosphate is well established, the role of these transmitters as putative trophic factors was investigated. Whereas noradrenaline was ineffective in preventing morphological changes due to denervation, both adenosine and N-ethylcarboxamido-adenosine totally prevented them. In conscious rats, the adenosine receptor antagonist dipropylsulphophenylxantine (DPSPX) caused alterations of the blood vessel wall similar to those described for denervation. These results strongly suggest that adenosine is the trophic factor of sympathetic innervation.
对血管进行化学或手术性交感神经去神经支配会导致效应细胞发生显著变化。由于节后交感神经通过去甲肾上腺素和5'-三磷酸腺苷进行共同传递已得到充分证实，因此对这些递质作为假定营养因子的作用进行了研究。而去甲肾上腺素在预防去神经支配引起的形态学变化方面无效，腺苷和N-乙基羧酰胺基腺苷则完全可以预防这些变化。在清醒大鼠中，腺苷受体拮抗剂二丙基磺酰苯基黄嘌呤（DPSPX）引起的血管壁改变与去神经支配所描述的改变相似。这些结果有力地表明，腺苷是交感神经支配的营养因子。
