Hartrodt W, Orlow G, Brosowski K H, Gürke R
Biomed Biochim Acta. 1985;44(3):455-64.
The renal nerve activity plays an essential role in the stimulation of plasma renin activity (PRA), which may be involved in the pathomechanism of neurogenic hypertension after sino-aortic denervation (SAD). Therefore, studies were conducted on unanesthetized rabbits (10 animals; 3-4 kg) after bilateral carotid sinus denervation plus section of cervical aortic nerves and the patterns of blood pressure (BP), heart rate (HR), and PRA were measured after a single injection-dosis of Saralasin (i.v., 10 micrograms/kg). After SAD the BP increased rapidly to 190 mm Hg within one week and remained at this high level (190-220 mm Hg) throughout the whole experiment (120 weeks). No change in BP of control rabbits (100-110 mm Hg) could be observed. Two weeks after SAD, the PRA showed a short elevation (approx. 25 ng) which subsequently returned to the levels of control rabbits (approx. 19 ng). Only in hypertensive rabbits Saralasin produced a short decrease of BP during both the initial and the whole chronic phases of hypertension, which was associated with a larger decrease of HR (1st to 5th min). Surprisingly, Saralasin induced a drop of HR also in the control rabbits. Our results suggest that also the normalized renin-angiotensin system is involved in the pathomechanism of sympathetic induced SAD-hypertension and probable permanently support the chronic state of hypertension by a relative "reninism".
肾神经活动在刺激血浆肾素活性（PRA）中起重要作用，这可能参与了去窦主动脉神经支配（SAD）后神经源性高血压的发病机制。因此，对双侧颈动脉窦去神经支配加颈主动脉神经切断后的未麻醉家兔（10只动物，体重3 - 4千克）进行了研究，并在单次静脉注射沙拉新（10微克/千克）后测量了血压（BP）、心率（HR）和PRA的变化模式。SAD后，血压在一周内迅速升至190毫米汞柱，并在整个实验（120周）中维持在这一高水平（190 - 220毫米汞柱）。对照家兔的血压（100 - 110毫米汞柱）未见变化。SAD后两周，PRA出现短暂升高（约25纳克），随后恢复到对照家兔的水平（约19纳克）。仅在高血压家兔中，沙拉新在高血压的初始和整个慢性阶段均使血压短暂下降，同时心率下降幅度更大（第1至5分钟）。令人惊讶的是，沙拉新在对照家兔中也引起了心率下降。我们的结果表明，正常化的肾素 - 血管紧张素系统也参与了交感神经诱导的SAD高血压的发病机制，并可能通过相对的“肾素血症”永久支持高血压的慢性状态。
