Zini S, Demassey Y, Fournié-Zaluski M C, Bischoff L, Corvol P, Llorens-Cortès C, Sanderson P
INSERM U 36, Collège de France, Paris.
Neuroreport. 1998 Mar 30;9(5):825-8. doi: 10.1097/00001756-199803300-00011.
The brain angiotensin (Ang) system plays an important role in the central control of vasopressin release. Using EC33, a selective aminopeptidase A inhibitor which blocks the metabolism of Ang II in Ang III, we previously reported that vasopressin release was under the control of Ang III and not Ang II. To determine accurately the action of EC33, the effects of intracerebroventricular injection of Ang peptides or EC33 on extracellular unit activity of vasopressinergic neurons in the supraoptic nucleus of urethane-anaesthetized rats were examined. Angiotensin II (15-30 ng) or Ang III (15 ng) increased the firing rate of all neurons tested. Conversely, EC33 (10 microg) reduced or completely abolished (30-60 microg) the basal firing rate for 4-6 min in all eight neurons tested. EC33 (30 microg) also inhibited the activity induced by 30 ng Ang II. It was concluded that the observed activity of Ang II required its conversion to Ang III and that endogenous Ang III may exert a tonic control on the basal firing level of vasopressinergic neurons.
脑内血管紧张素（Ang）系统在血管升压素释放的中枢控制中起重要作用。使用EC33（一种选择性氨肽酶A抑制剂，可阻断Ang II向Ang III的代谢），我们先前报道血管升压素的释放受Ang III而非Ang II的控制。为了准确确定EC33的作用，研究了脑室内注射Ang肽或EC33对氨基甲酸乙酯麻醉大鼠视上核中血管升压素能神经元细胞外单位活动的影响。血管紧张素II（15 - 30 ng）或血管紧张素III（15 ng）增加了所有测试神经元的放电频率。相反，在所有测试的8个神经元中，EC33（10微克）使基础放电频率降低或在4 - 6分钟内完全消除（30 - 60微克）。EC33（30微克）也抑制了30 ng血管紧张素II诱导的活动。得出的结论是，观察到的血管紧张素II的活性需要将其转化为血管紧张素III，并且内源性血管紧张素III可能对血管升压素能神经元的基础放电水平发挥紧张性控制作用。
