Egan B, Fitzpatrick M A, Julius S
Circulation. 1987 Jan;75(1 Pt 2):I130-3.
The cause of the low-renin state in hypertension is unknown. To consider our hypothesis that cardiopulmonary mechanoreceptors suppress renin release in these patients, it was necessary to prove that "low pressure" receptors affected renin levels in man. A series of experiments was performed to selectively alter the stretch (load) on carotid and cardiopulmonary baroreceptors in healthy human volunteers. These studies showed that selectively altering high-pressure baroreceptor load did not affect plasma renin activity. Selectively unloading the low-pressure receptors increased plasma renin activity. Simultaneous unloading of both baroreceptors caused the largest increases in renin activity. While the data indicated an interaction of high- and low-pressure receptors on the neural regulation of renin release, we interpreted these results as evidence for a predominant influence of cardiopulmonary mechanoreceptors on the neurogenic regulation of renin secretion in man.
高血压患者低肾素状态的原因尚不清楚。为了验证我们的假设,即心肺机械感受器抑制这些患者的肾素释放,有必要证明“低压”感受器会影响人体的肾素水平。我们对健康人类志愿者进行了一系列实验,以选择性地改变颈动脉和心肺压力感受器的牵张(负荷)。这些研究表明,选择性改变高压压力感受器负荷不会影响血浆肾素活性。选择性卸载低压感受器会增加血浆肾素活性。同时卸载两种压力感受器会使肾素活性增加幅度最大。虽然数据表明高压和低压感受器在肾素释放的神经调节上存在相互作用,但我们将这些结果解释为心肺机械感受器对人体肾素分泌的神经源性调节具有主要影响的证据。