Grassi G, Giannattasio C, Cuspidi C, Bolla G B, Cléroux J, Ferrazzi P, Fiocchi R, Mancia G
Instituto di Clinica Medica Generale e Terapia Medica, Università di Milano, Italy.
Am J Med. 1988 Mar 11;84(3A):97-104. doi: 10.1016/0002-9343(88)90212-4.
Cardiopulmonary receptors have been shown to modulate renin release in animals. However, their involvement in reflex control of renin in humans has never been unequivocally established. This report reviews data on the effects on plasma renin activity of maneuvers (lower body negative pressure and passive leg raising) that reduce and increase central venous pressure and cardiac diameter without affecting blood pressure and heart rate, thereby deactivating and stimulating cardiopulmonary receptors with little or no involvement of the arterial baroreceptors. In normotensive subjects, reduction in central venous pressure was accompanied by an increase in plasma renin activity that was similar to the increase observed during tilt that reduced central venous pressure to a similar extent. Conversely, an increase in central venous pressure was accompanied by a reduction in plasma renin activity. The increase in plasma renin activity that followed the reduction in central venous pressure was drastically attenuated in four patients who had undergone cardiac transplantation, along with other reflex effects (changes in forearm vascular resistance and plasma norepinephrine) of cardiopulmonary receptor manipulations. There was a modest reduction in the overall reflex changes in plasma renin activity in patients with mild to moderate essential hypertension compared with normotensive subjects. However, patients with essential hypertension and cardiac hypertrophy showed marked attenuation of all reflex influences of the cardiopulmonary receptors. In five subjects, therapeutic regression of this structural alteration was associated with a clear improvement in the cardiopulmonary reflex. Thus, in humans, cardiopulmonary receptors exert an important reflex control of renin release. This control (which is due in part to receptors located in the cardiac walls) is moderately affected by a mild to moderate blood pressure elevation but is markedly impaired when the elevation produces structural alterations in the heart. Preliminary evidence, however, suggests that the cardiopulmonary reflex may be improved by a reduction in cardiac hypertrophy.
心肺感受器已被证明可调节动物体内肾素的释放。然而，它们在人类肾素反射控制中的作用尚未得到明确证实。本报告回顾了关于降低和升高中心静脉压及心脏直径而不影响血压和心率的操作（下体负压和被动抬腿）对血浆肾素活性影响的数据，从而在很少或没有动脉压力感受器参与的情况下使心肺感受器失活和激活。在血压正常的受试者中，中心静脉压降低伴随着血浆肾素活性增加，这与在倾斜过程中观察到的中心静脉压降低到类似程度时的增加相似。相反，中心静脉压升高伴随着血浆肾素活性降低。在接受心脏移植的四名患者中，中心静脉压降低后血浆肾素活性的增加以及心肺感受器操作的其他反射效应（前臂血管阻力和血浆去甲肾上腺素的变化）都显著减弱。与血压正常的受试者相比，轻度至中度原发性高血压患者血浆肾素活性的总体反射变化有适度降低。然而，原发性高血压和心脏肥大患者的心肺感受器的所有反射影响均显著减弱。在五名受试者中，这种结构改变的治疗性消退与心肺反射的明显改善有关。因此，在人类中，心肺感受器对肾素释放发挥重要的反射控制作用。这种控制（部分归因于位于心脏壁上的感受器）受到轻度至中度血压升高的适度影响，但当血压升高导致心脏结构改变时则明显受损。然而，初步证据表明，心脏肥大的减轻可能会改善心肺反射。
