Richardson J B, Beaulnes A
J Cell Biol. 1971 Nov;51(21):419-32. doi: 10.1083/jcb.51.2.419.
The site of action and the distribution of angiotensin II have been studied in the mouse. A comparison of the ratios of angiotensin-(14)C and inulin-(3)H at the time of the pressor effect reveals an extracellular pattern of distribution. Morphological studies were made using angiotensin coupled to exogenous enzymes which can be demonstrated histochemically. Coupling of angiotensin to horseradish peroxidase or cytochrome c, with glutaraldehyde or difluorodinitrodiphenylsulfone (FNPS) as the coupling agent, does not alter the pattern of its vasopressor response or that of its inactivation; nor are differences present between angiotensin and the angiotensin-enzyme complexes in the stimulation of in vitro tissue preparations. Dissociation of the complexes was shown not to occur in vitro, but the possibility of a serum factor splitting the complexes immediately after intravenous injection cannot be excluded. Since these complexes are localized on the endothelium and not on the smooth muscle at the time of maximum hypertension, the endothelium is proposed as the site of action for angiotensin.
已在小鼠体内研究了血管紧张素II的作用部位和分布情况。在出现升压效应时，对血管紧张素-(14)C与菊粉-(3)H的比率进行比较，结果显示其分布呈细胞外模式。利用与可通过组织化学方法进行示踪的外源性酶偶联的血管紧张素进行了形态学研究。以戊二醛或二氟二硝基二苯砜（FNPS）作为偶联剂，将血管紧张素与辣根过氧化物酶或细胞色素c偶联，并不会改变其升压反应模式或失活模式；在体外组织制备物的刺激方面，血管紧张素与血管紧张素-酶复合物之间也不存在差异。已证明复合物在体外不会发生解离，但不能排除静脉注射后血清因子立即裂解复合物的可能性。由于在血压最高时这些复合物定位于内皮细胞而非平滑肌，因此推测内皮细胞是血管紧张素的作用部位。
