Miklós E S, Juhász-Nagy A
Acta Physiol Hung. 1984;63(2):161-5.
Calcium-dependence of the adenosine-induced renal vasoconstriction was studied in dogs anaesthetized with pentobarbital. Close intraarterial (i.a.) infusion of adenosine (40 and 100 micrograms X min-1) elicited a significant blood flow decrease followed by partial recovery during the 2 min infusion periods as measured with an electromagnetic flow probe. I.a. infusion of verapamil (100 micrograms X min-1) blocked the constrictor response. Verapamil also reduced the vasoconstriction produced by i.a. angiotensin II (0.1 micrograms X min-1) or adrenaline (0.6 micrograms X min-1). Blood pressure remained unchanged throughout all the interventions. The results indicate that the adenosine-induced renal vascular response depends on the availability of extracellular Ca2+ to the contractile mechanism of smooth muscle, a property shared by other well known renal constrictor agents.
在戊巴比妥麻醉的犬中研究了腺苷诱导的肾血管收缩的钙依赖性。通过电磁流量探头测量，在2分钟输注期间，动脉内（i.a.）密切输注腺苷（40和100微克×分钟-1）引起显著的血流减少，随后部分恢复。动脉内输注维拉帕米（100微克×分钟-1）可阻断收缩反应。维拉帕米还可减轻动脉内输注血管紧张素II（0.1微克×分钟-1）或肾上腺素（0.6微克×分钟-1）所产生的血管收缩。在所有干预过程中血压均保持不变。结果表明，腺苷诱导的肾血管反应取决于细胞外Ca2+对平滑肌收缩机制的可用性，这是其他知名肾血管收缩剂共有的特性。
