Virdis A, Ghiadoni L, Favilla S, Duranti P, Taddei S, Salvetti A
Department of Internal Medicine, University of Pisa, Italy.
Blood Press. 1999;8(2):85-93. doi: 10.1080/080370599438257.
A vascular renin-angiotensin system (RAS) is present in the forearm vasculature of essential hypertensive patients and is closely related to the circulating renin profile. To test whether the haemodynamic effect of acute intrabrachial administration of captopril is related to the circulating and/or vascular RAS, 31 hypertensive patients were selected and divided into four groups according to their different circulating RAS profile (n = 7 hypertensive patients with primary aldosteronism and suppressed plasma renin activity; n = 7 low renin essential hypertensive patients; n = 8 normal renin essential hypertensive patients; n = 9 high renin renovascular hypertensive patients). The forearm net balance of active renin, plasma renin activity and angiotensin II, obtained by intrabrachial infusion of the beta-adrenergic receptor agonist isoproterenol (0.03, 0.1, 0.3 microg/100 ml/min) and calculated as the product of the venous-arterial plasma concentration gradient and forearm blood flow (FBF), was closely related to the circulating RAS. Captopril (0.25, 2.5, 25 microg/100 ml/min per 20 min each dose) unchanged basal FBF in the primary aldosteronism and low renin groups (FBF increase: from 3.9 +/- 0.4 to a maximum of 4.1 +/- 0.5 and from 3.8 +/- 0.3 to a maximum of 4.3 +/- 0.5 ml/100 ml/min, respectively), whereas it caused slight vasodilation in the normal renin group (from 3.9 +/- 0.3 to a maximum of 5.3 +/- 0.7 ml/100 ml/min), and pronounced vasodilation in the high renin group (from 4.0 +/- 0.4 to a maximum of 6.4 +/- 0.5 ml/100 ml/min). Captopril-induced vasodilation showed a significant direct correlation with the circulating and vascular RAS. The present data, while confirming the existence of a vascular RAS in the forearm of hypertensive patients indicate that the acute vasodilating effect of intrabrachial captopril is linked to a stimulated RAS, either circulating or vascular, supporting the evidence that, in acute conditions, ACE inhibitors exert their vasodilating effect through the RAS blockade.
血管紧张素系统（RAS）存在于原发性高血压患者的前臂血管中，且与循环肾素谱密切相关。为了测试急性肱动脉内给予卡托普利的血流动力学效应是否与循环和/或血管RAS相关，选取了31例高血压患者，并根据其不同的循环RAS谱分为四组（n = 7例原发性醛固酮增多症且血浆肾素活性受抑制的高血压患者；n = 7例低肾素原发性高血压患者；n = 8例正常肾素原发性高血压患者；n = 9例高肾素肾血管性高血压患者）。通过肱动脉内输注β-肾上腺素能受体激动剂异丙肾上腺素（0.03、0.1、0.3微克/100毫升/分钟）获得的前臂活性肾素、血浆肾素活性和血管紧张素II的净平衡，计算为静脉-动脉血浆浓度梯度与前臂血流量（FBF）的乘积，与循环RAS密切相关。卡托普利（每20分钟每剂量0.25、2.5、25微克/100毫升/分钟）在原发性醛固酮增多症和低肾素组中未改变基础FBF（FBF增加：分别从3.9±0.4增加到最大4.1±0.5以及从3.8±0.3增加到最大4.3±0.5毫升/100毫升/分钟），而在正常肾素组中引起轻微血管舒张（从3.9±0.3增加到最大5.3±0.7毫升/100毫升/分钟），在高肾素组中引起明显血管舒张（从4.0±0.4增加到最大6.4±0.5毫升/100毫升/分钟）。卡托普利诱导的血管舒张与循环和血管RAS呈显著正相关。目前的数据在证实高血压患者前臂存在血管RAS的同时表明，肱动脉内给予卡托普利的急性血管舒张作用与受刺激的RAS（循环或血管）相关，支持了在急性情况下血管紧张素转换酶抑制剂通过RAS阻断发挥其血管舒张作用的证据。
