Gavras H, Ribeiro A B, Gavras I, Brunner H R
N Engl J Med. 1976 Dec 2;295(23):1278-83. doi: 10.1056/NEJM197612022952302.
To investigate the roles of angiotensin II and sodium in essential high-renin, normal-renin and low-renin hypertension, 14 patients received the competitive antagonist of angiotensin II, saralasin, during periods of sodium depletion and repletion. Blood-pressure response to saralasin was determined by the state of sodium balance. Patients from all three renin subgroups exhibited a fall in blood pressure when sufficiently sodium depleted, and an elevation in blood pressure when sodium replete or insufficiently depleted. However, those with low renin required loss of substantially more sodium (sufficient to elicit compensatory stimulation of renin) before depletion could be achieved. In patients with essential hypertension of all three renin subgroups, sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. Even the low-renin type can become renin dependent with sufficient sodium depletion.
为研究血管紧张素II和钠在原发性高肾素、正常肾素和低肾素性高血压中的作用，14例患者在钠缺失和补充期间接受了血管紧张素II竞争性拮抗剂沙拉新。对沙拉新的血压反应由钠平衡状态决定。来自所有三个肾素亚组的患者在钠充分缺失时血压下降，而在钠充足或缺失不足时血压升高。然而，低肾素患者在达到钠缺失之前需要丢失更多的钠（足以引发肾素的代偿性刺激）。在所有三个肾素亚组的原发性高血压患者中，钠平衡决定了肾素-血管紧张素系统在维持高血压中的参与程度。即使是低肾素型患者，在充分的钠缺失情况下也会变得依赖肾素。
