Morganti A, Grassi G, Sala C, Capozi A, Turolo L, Sabadini E, Bolla G, Mancia G, Zanchetti A
Istituto di Clinica Medica IV, Università di Milano, Italy.
J Hypertens Suppl. 1985 Dec;3(3):S259-62.
Several lines of evidence indicate that angiotensin II (ANG II) may potentiate the vascular response to sympathetic stimulation. However, there are no clear signs that this action of ANG II is physiologically relevant in man. To investigate this problem, we used the lower body negative pressure technique (LBNP, -15 mmHg) to deactivate cardiopulmonary receptors and reflexly stimulate the sympathetic nervous system. The haemodynamic (changes in blood pressure, heart rate, central venous pressure, forearm blood flow) and humoral effects [changes in plasma noradrenaline (PNA) and plasma renin activity (PRA)] of this manoeuvre were examined before and after blockade of angiotensin formation achieved by the administration of the converting enzyme inhibitor, captopril. Studies were performed in patients with essential hypertension in control conditions and after acute and chronic captopril treatment. We found that the reduction in forearm blood flow induced by LBNP was significantly diminished after acute and chronic captopril in spite of the fact that the fall in central venous pressure and the increases in PNA were similar to those observed in control conditions. In contrast, the response of renin to LBNP was enhanced, at least after acute captopril administration. These findings suggest that efficiency of the reflexes originating from the cardiopulmonary receptors is impaired after captopril. Angiotensin II contributes to the vasoconstrictive ability of the sympathetic nervous system, either through a direct vascular action or by enhancing the vascular responsiveness to noradrenaline stimulation. However, this sympathetic facilitatory action of ANG II does not appear to be extended on the adrenergic mechanisms which regulate renin release.
多条证据表明，血管紧张素II（ANG II）可能增强血管对交感神经刺激的反应。然而，尚无明确迹象表明ANG II的这一作用在人体中具有生理相关性。为了研究这个问题，我们采用下体负压技术（LBNP，-15 mmHg）来使心肺感受器失活并反射性刺激交感神经系统。在给予转化酶抑制剂卡托普利以阻断血管紧张素形成之前和之后，检测了该操作的血流动力学（血压、心率、中心静脉压、前臂血流量的变化）和体液效应[血浆去甲肾上腺素（PNA）和血浆肾素活性（PRA）的变化]。在原发性高血压患者处于对照状态时以及急性和慢性卡托普利治疗后进行了研究。我们发现，尽管中心静脉压下降以及PNA升高与对照状态下观察到的情况相似，但急性和慢性卡托普利治疗后，LBNP诱导的前臂血流量减少明显减轻。相反，至少在急性给予卡托普利后，肾素对LBNP的反应增强。这些发现表明，卡托普利治疗后源自心肺感受器的反射效率受损。血管紧张素II通过直接的血管作用或通过增强血管对去甲肾上腺素刺激的反应性，有助于交感神经系统的血管收缩能力。然而，ANG II的这种交感促进作用似乎并未扩展到调节肾素释放的肾上腺素能机制上。
