Autonomic and baroreflex function after captopril in hypertension.

Autonomic and baroreflex function after captopril in hypertension.
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卡托普利治疗高血压后的自主神经和压力反射功能。

DOI:
10.1016/0002-8703(83)90403-9
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发表时间:
1983
影响因子:
4.8
通讯作者:
Cohen,IM
Cohen,IM
中科院分区:
医学2区
文献类型:
--
作者:
Warren,SE;O'Connor,DT;Cohen,IM

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卡托普利治疗无反射性心动过速提示循环反射减弱,可能有助于降压效果,血管紧张素转换酶抑制可能改变交感神经功能。观察卡托普利对5例重度高血压患者自主神经功能的影响。所有患者的平均血压下降(从141±6到119±7毫米汞柱,p< 0.02),卡托普利治疗后直立血压未下降或心率升高(均为0.0.1)。卡托普利对亚硝酸盐戊酯低血压或苯肾上腺素高血压(均为>.1)的压力反射敏感性没有改变。将这些严重高血压患者与年龄匹配的正常血压对照组进行比较,结果显示,在亚硝酸盐戊酯试验(89%,p< 0.01)和苯肾上腺素试验(83%,p< 0.01)中,压力反射敏感性均明显减弱,这表明压力反射功能的基线减弱可能部分解释了反射性心动过速的消失。卡托普利降低了冷应激后的心加速(从61±38毫秒降至23±43毫秒,p< 0.05)以及α -肾上腺素能阻断后的血压下降(从46±13毫米汞柱降至24±9毫米汞柱,p< 0.05),提示交感神经对阻力血管的刺激减少,交感神经对血压维持的参与减少,可能是在突触前水平。交感神经活动的4项生化指标没有变化。因此,卡托普利治疗的患者有反射性心动过速钝化,与基线时的barreflex功能钝化相当,并且通过卡托普利治疗获得了交感神经活动减弱的生理和药理学证据。是否减少交感神经活动参与卡托普利的降压作用尚未确定。
Absent reflex tachycardia with captopril therapy suggests blunting of circulatory reflexes, perhaps contributing to antihypertensive efficacy, and angiotensin converting enzyme inhibition may alter sympathetic function. Captopril effects on autonomic function were investigated in five severe hypertensive patients. Mean blood pressure fell in all patients (from 141 ± 6 to 119 ± 7 mm Hg,p< 0.02) without orthostatic blood pressure fall or increase in heart rate (bothp> 0.1) on captopril. Captopril did not alter baroreflex sensitivity as tested by amyl nitrite hypotension or phenylephrine hypertension (bothp> 0.1). Comparison of these severely hypertensive patients to age matched normotensive control subjects did reveal markedly blunted baroreflex sensitivity in both the amyl nitrite test (by 89%,p< 0.01) and the phenylephrine test (by 83%,p< 0.01), suggesting that baseline blunting of baroreflex function may in part account for absence of reflex tachycardia. Captopril diminished the cardioacceleration after cold stress (from 61 ± 38 to 23 ± 43 msec,p< 0.05) as well as the blood pressure fall after alpha-adrenergic blockade (from 46 ± 13 to 24 ± 9 mm Hg,p< 0.05), suggesting diminished sympathetic stimulation of resistance vessels and decreased sympathetic participation in blood pressure maintenance, possibly at the prejunctional synpatic level. Four biochemical indices of sympathetic activity did not change. Thus captopril-treated patients had blunted reflex tachycardia, commensurate with blunted baroreflex function at baseline, and physiologic and pharmacologic evidence of diminished sympathetic activity was obtained with captopril therapy. Whether diminished sympathetic activity is involved in captopril's antihypertensive effect has not been determined.
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