Torikai S
National Cardiovascular Center, Department of Pharmacology, Osaka, Japan.
Ren Physiol. 1987;10(1):33-9. doi: 10.1159/000173111.
To test the possibility that adenosine may be involved in a urine concentrating mechanism, effects of 1-phenylisopropyladenosine (PIA) on cyclic AMP levels have been examined in medullary thick ascending limb (mTAL) and medullary collecting duct (MCD) isolated from the rat. Low and high doses of PIA did not alter basal cyclic AMP levels in both segments. However, PIA depressed vasopressin-dependent cyclic AMP production in MCD in a dose-dependent manner: this effect of PIA was maximum at 10(-6) M. 8-Phenyltheophylline, a competitive inhibitor for adenosine receptor, completely abolished this inhibitory effect of PIA. This finding may suggest an existence of adenosine receptor on the MCD. In mTAL, PIA also suppressed vasopressin-mediated cyclic AMP generation. The present study shows an interaction between PIA and vasopressin in both MCD and mTAL. This interaction may contribute in part to urinary-concentrating disturbance in renal ischemia.
为了测试腺苷可能参与尿液浓缩机制的可能性，研究了1-苯基异丙基腺苷（PIA）对从大鼠分离出的髓袢升支粗段（mTAL）和髓质集合管（MCD）中环磷酸腺苷（cAMP）水平的影响。低剂量和高剂量的PIA均未改变这两个节段的基础cAMP水平。然而，PIA以剂量依赖的方式抑制了MCD中血管加压素依赖性cAMP的产生：PIA的这种作用在10^(-6) M时最大。8-苯基茶碱是一种腺苷受体竞争性抑制剂，它完全消除了PIA的这种抑制作用。这一发现可能提示MCD上存在腺苷受体。在mTAL中，PIA也抑制了血管加压素介导的cAMP生成。本研究显示了PIA与血管加压素在MCD和mTAL中的相互作用。这种相互作用可能部分导致肾缺血时的尿液浓缩障碍。
