Uza G
Med Interne. 1976 Apr-Jun;14(2):87-96.
The vasopressor response to angiotensin II was found useful in the differential diagnosis of arterial hypertension and for a better understanding of its pathogenesis. Sodium supply was proved to influence significantly the pressor response to angiotensin II and not that to noradrenaline thus implying the presence of arterial receptors which bind angiotensin specifically. Angiotensin caused an increase of the urinary excretion of electrolytes in hypertensive patients and a decreased electrolyte excretion in normotensives. In most hypertensive patients angiotensin was found to decrease the plasma angiotensinogen and to activate the bradykinin-bradykininogen and fibrinolytic systems. In the presence of urinary infection angiotensin increased the platelet adhesiveness and the thrombelastographic changes proved that in this condition angiotensin increases the tendency to thrombosis.
血管紧张素II的升压反应在动脉高血压的鉴别诊断以及更好地理解其发病机制方面被证明是有用的。事实证明，钠供应会显著影响对血管紧张素II的升压反应，而对去甲肾上腺素的升压反应则无影响，这意味着存在特异性结合血管紧张素的动脉受体。血管紧张素可使高血压患者的电解质尿排泄增加，而使血压正常者的电解质排泄减少。在大多数高血压患者中，发现血管紧张素可降低血浆血管紧张素原，并激活缓激肽-缓激肽原和纤溶系统。在存在泌尿系统感染的情况下，血管紧张素会增加血小板黏附性，血栓弹力图变化证明在这种情况下血管紧张素会增加血栓形成倾向。
