Xu B, Chen R X, Chen D G, Zhang L, Li J M
Cardiovascular Research Unit, Nanjing Railway Medical College, Nanjing, China.
Zhongguo Yao Li Xue Bao. 1990 Sep;11(5):438-41.
Experimental renal hypertensive and normal dogs with femoral arteries constantly perfused were studied. Cocaine was used to block the presynaptic norepinephrine (NE) reuptake and tyramine to initiate the release of NE in sympathetic nerve endings. NE spillover and infusion pressure were measured under basic conditions and during intraarterial infusion of cocaine, tyramine and in combination with alpha 1 and alpha 2 adrenoceptor antagonists. The extent of NE spillover increase induced by infusion of tyramine, the increased infusion pressure by cocaine and tyramine, and the reduced infusion pressure by prazosin were all greater in hypertensive dogs than those in normal dogs, but adrenoceptor antagonist idazoxan further increased tyramine-induced NE spillover in normal dogs only. It was suggested that reduced-regulation of presynaptic alpha 2 adrenoceptors to NE release and increased responsiveness of postsynaptic alpha 1 adrenoceptors to NE were present in hypertensive dogs.
对股动脉持续灌注的实验性肾性高血压犬和正常犬进行了研究。使用可卡因阻断突触前去甲肾上腺素（NE）的再摄取，并使用酪胺引发交感神经末梢NE的释放。在基础条件下以及动脉内输注可卡因、酪胺以及与α1和α2肾上腺素能受体拮抗剂联合使用时，测量NE溢出量和灌注压力。酪胺输注引起的NE溢出增加程度、可卡因和酪胺引起的灌注压力升高以及哌唑嗪引起的灌注压力降低在高血压犬中均比正常犬更大，但肾上腺素能受体拮抗剂咪唑克生仅在正常犬中进一步增加了酪胺诱导的NE溢出。研究表明，高血压犬存在突触前α2肾上腺素能受体对NE释放的调节降低以及突触后α1肾上腺素能受体对NE的反应性增加。
