Mancia G, Giannattasio C, Grassi G, Morganti A, Zanchetti A
Cattedra di Semeiotica Medica e Istituto di Clinica Medica, Università di Milano, Italy.
J Hypertens Suppl. 1988 Dec;6(3):S45-9.
Removal of the facilitating effect of angiotensin II on sympathetic cardiovascular influences may enhance the antihypertensive effect of angiotensin converting enzyme (ACE) inhibitors but may also disturb reflexes involved in blood pressure homeostasis. To test this hypothesis in essential hypertensive subjects, the forearm vasomotor response to cardiopulmonary receptor deactivation (lower body negative pressure) was studied before and after acute or prolonged administration of captopril at doses capable of lowering blood pressure and blocking the formation of angiotensin II. After either acute or prolonged captopril administration there was less response (i.e. forearm vasoconstriction) than in the no-drug state. However, in the same subjects, another reflex response to cardiopulmonary receptor deactivation, the increase in plasma renin activity, was not blunted by the drug. Furthermore, the other major reflex responsible for blood pressure homeostasis, the arterial baroreflex, was left unchanged or was even favoured by administration of clinically effective doses of captopril. This finding applied to both the heart rate and the blood pressure modulating ability of the reflex (vasoactive drug and neck chamber techniques, respectively). Thus, reflex control of circulation may be adversely affected by ACE inhibition. However, this does not include all reflex targets and at least one major reflex is preserved following this pharmacological intervention. This may explain why our patients showed no orthostatic hypotension during chronic treatment with ACE inhibitors.
消除血管紧张素II对交感神经心血管影响的促进作用，可能会增强血管紧张素转换酶（ACE）抑制剂的降压效果，但也可能干扰参与血压稳态的反射。为了在原发性高血压患者中验证这一假设，研究了在急性或长期给予能够降低血压并阻断血管紧张素II形成的剂量的卡托普利前后，前臂血管运动对心肺感受器失活（下体负压）的反应。在急性或长期给予卡托普利后，与无药物状态相比，反应（即前臂血管收缩）较小。然而，在同一受试者中，对心肺感受器失活的另一种反射反应，即血浆肾素活性的增加，并未被药物减弱。此外，负责血压稳态的另一个主要反射，即动脉压力反射，在给予临床有效剂量的卡托普利后保持不变，甚至得到促进。这一发现适用于反射对心率和血压的调节能力（分别采用血管活性药物和颈静脉技术）。因此，ACE抑制可能会对循环的反射控制产生不利影响。然而，这并不包括所有反射靶点，并且在这种药物干预后至少有一个主要反射得以保留。这可能解释了为什么我们的患者在使用ACE抑制剂进行慢性治疗期间没有出现体位性低血压。
