MacDermot J, Barnes P J
Eur J Pharmacol. 1980 Oct 31;67(4):419-25. doi: 10.1016/0014-2999(80)90183-1.
Prostacyclin activates adenylate cyclase of guinea pig lung homogenates. The concentration for half-maximum activation was 20 nM. Kinetic analysis of the increase in enzyme activity suggested a non-cooperative, bimolecular interaction between prostacyclin and a single receptor population. Comparison of the activity of prostacyclin with that of other prostaglandins revealed a rank order of potency: prostacyclin > prostaglandin E1 > prostaglandin E2 > prostaglandin F1 alpha. 6-Oxo-prostaglandin F1 alpha, the stable hydrolysis product of prostacyclin, produced no increase in adenylate cyclase activity. Lungs were dissected before homogenisation, and prostacyclin-sensitive adenylate cyclase was identified at high concentrations in peripheral lung tissue containing small airways, blood vessels and parenchyma. The precise cellular location of these receptors remains obscure, but the probability that they are in the pulmonary vascular bed rather than airway smooth muscle is discussed.
前列环素可激活豚鼠肺匀浆中的腺苷酸环化酶。半数最大激活浓度为20 nM。对酶活性增加的动力学分析表明，前列环素与单一受体群体之间存在非协同的双分子相互作用。将前列环素与其他前列腺素的活性进行比较，得出效力顺序为：前列环素>前列腺素E1>前列腺素E2>前列腺素F1α。6-氧代前列腺素F1α是前列环素的稳定水解产物，不会使腺苷酸环化酶活性增加。在匀浆前解剖肺脏，在含有小气道、血管和实质的外周肺组织中，高浓度时可鉴定出对前列环素敏感的腺苷酸环化酶。这些受体的确切细胞定位仍不清楚，但文中讨论了它们存在于肺血管床而非气道平滑肌中的可能性。
