Devynck M A, Meyer P
Am J Med. 1976 Nov;61(5):758-67. doi: 10.1016/0002-9343(76)90157-1.
The biologic effect of angiotensin II is triggered by its interaction with components of target organs, which specifically recognize the hormone. These receptors have been studied with the use of radioactive angiotensin and, as for other peptidic hormones, have been localized in the plasma membrane of target cells. Such angiotensin receptors have been characterized in three target organs: vascular tissue, uterus and adrenal cortex. The binding characteristics differ in contractile tissue and in adrenal glands, the N and C terminal ends of angiotensin being involved in the former, whereas the N terminus does not appear to have the same importance in the latter. Numerous factors, including ionic composition, seem to be able to modify angiotensin-receptor interaction in vascular smooth muscle. However, the molecular mechanisms responsible for angiotensin binding and for the transmission of the signal determined by receptor-angiotensin interaction are not yet understood. As observed with other peptidic hormones, the number of angiotensin receptors seems to be susceptible to variation under certain conditions. In uterine smooth muscle, it was shown that the number of receptors increased after nephrectomy, a phenomenon which was prevented by the prolonged infusion of angiotensin. The significance of such a variation remains unknown, but it may be partially responsible for the inverse relationship that exists between the endogenous angiotensin level and the pressor effect of exogenous angiotensin. In the near future, investigation of the angiotensin-receptor mechanism will probably answer whether the variation in angiotensin receptors is similar in all target tissues and whether an angiotensin-receptor mechanism is involved in the pathogenesis of certain varieties of hypertension. In addition, a precise understanding of the angiotensin-receptor interaction with help the development of new angiotensin antagonists.
血管紧张素II的生物学效应是由其与靶器官成分相互作用引发的，这些靶器官成分能特异性识别该激素。人们利用放射性血管紧张素对这些受体进行了研究，与其他肽类激素一样，已将其定位在靶细胞的质膜中。这种血管紧张素受体已在三个靶器官中得到表征：血管组织、子宫和肾上腺皮质。收缩组织和肾上腺中的结合特性有所不同，血管紧张素的N端和C端参与前者的作用，而N端在后者中似乎不具有同样的重要性。许多因素，包括离子组成，似乎都能改变血管平滑肌中血管紧张素与受体的相互作用。然而，血管紧张素结合以及由受体 - 血管紧张素相互作用所决定的信号传递的分子机制尚不清楚。正如在其他肽类激素中所观察到的那样，血管紧张素受体的数量在某些条件下似乎易于发生变化。在子宫平滑肌中，研究表明肾切除术后受体数量增加，而这种现象可通过长期输注血管紧张素得以预防。这种变化的意义尚不清楚，但它可能部分解释了内源性血管紧张素水平与外源性血管紧张素升压效应之间存在的反比关系。在不久的将来，对血管紧张素受体机制的研究可能会回答血管紧张素受体在所有靶组织中的变化是否相似，以及血管紧张素受体机制是否参与某些类型高血压的发病过程。此外，对血管紧张素与受体相互作用的精确了解将有助于开发新的血管紧张素拮抗剂。
