Ackerly J A, Felger T S, Peach M J
Eur J Pharmacol. 1976 Jul;38(1):113-21. doi: 10.1016/0014-2999(76)90207-7.
The administration of radioactive angiotensin I to the retrogradely perfused feline adrenal gland caused a brisk discharge of catecholamines. Recovery of the labelled decapeptide and metabolites in the adrenal effluent fluid was complete in 5 min. Radioimmunoassay of this perfusate revealed that most of the peptide remained as angiotensin I, but chromatographic and electrophoretic evaluation indicated that greater than 68% of the peptide had been metabolized to des-asp1 -angiotensin I. The absence of des-asp1 -angiotensin II, angiotensin II or his-3H-leu in adrenal effluent fluid suggested minimal dipeptidyl carboxypeptidase activity in this preparation. In addition, the profile of angiotensin I metabolites from the perfused adrenal was not altered by treatment with a converting enzyme inhibitor B. jararaca nonapeptide. The des-asp1-angiotensin I peptide was a very weak secretagogue in the adrenal medulla. If metabolism of the decapeptide to the nonapeptide occurs in the medulla, this may represent a pathway to limit the secretory action of angiotensin I. These results suggest a high degree of adrenal aminopeptidase activity which may be primarily localized in the adrenal cortex.
向逆行灌注的猫肾上腺注射放射性血管紧张素I可引起儿茶酚胺的快速释放。5分钟内肾上腺流出液中标记的十肽及其代谢产物完全回收。对该灌注液进行放射免疫分析发现，大部分肽仍为血管紧张素I，但色谱和电泳分析表明，超过68%的肽已代谢为去天冬氨酸1 -血管紧张素I。肾上腺流出液中不存在去天冬氨酸1 -血管紧张素II、血管紧张素II或组氨酸-3H-亮氨酸，表明该制剂中肽基羧肽酶活性极低。此外，灌注肾上腺产生的血管紧张素I代谢产物谱不会因用转化酶抑制剂B. jararaca九肽处理而改变。去天冬氨酸1 -血管紧张素I肽在肾上腺髓质中是一种非常弱的促分泌剂。如果十肽在髓质中代谢为九肽，这可能是限制血管紧张素I分泌作用的一条途径。这些结果表明肾上腺氨肽酶活性很高，可能主要定位于肾上腺皮质。
