Mills P J, Dimsdale J E, Ziegler M G, Hauger R L, Nelesen R A, Brown M R
Department of Medicine, University of California, San Diego Medical Center 92103-0804.
J Am Coll Cardiol. 1993 Jan;21(1):177-81. doi: 10.1016/0735-1097(93)90734-i.
The purpose of this study was to examine the effects of short-term captopril therapy during sodium restriction on several markers of the sympathetic nervous system, including plasma norepinephrine, neuropeptide Y, beta-adrenergic receptors and cortisol.
Recent studies suggest that the therapeutic effects of converting enzyme inhibitors involve not only the renin-angiotensin and prostaglandin systems but also the sympathetic system.
Twelve hypertensive and 20 normotensive men were studied after 2 5-day hospital stays during which they consumed a 10-mEq sodium diet and received captopril (25 mg twice daily) or placebo in a double-blind crossover study.
Captopril decreased neuropeptide Y (p < 0.05) and angiotensin II (p < 0.01) and increased isoproterenol-stimulated cyclic adenosine monophosphate (AMP) in lymphocytes (p < 0.03), plasma norepinephrine (p < 0.02), cortisol (p < 0.05) and renin (p < 0.001) in both hypertensive and normotensive subjects. Hypertensive subjects had an increased beta-adrenergic receptor density (p < 0.02) and a greater decrease in diastolic blood pressure compared with normotensive subjects (p < 0.02).
The results of this study suggest that the short-term therapeutic effects of captopril may involve concerted changes in key components of the sympathetic nervous system. These findings, such as decreased neuropeptide Y combined with increased norepinephrine and beta-adrenergic receptors, are compatible with the observation of increased cardiac output and decreased peripheral resistance after short-term angiotensin-converting enzyme inhibition.
本研究旨在探讨短期卡托普利治疗在限钠期间对交感神经系统的几个标志物的影响，这些标志物包括血浆去甲肾上腺素、神经肽Y、β-肾上腺素能受体和皮质醇。
最近的研究表明，转换酶抑制剂的治疗作用不仅涉及肾素-血管紧张素和前列腺素系统，还涉及交感神经系统。
对12名高血压男性和20名血压正常男性进行了研究，他们在住院2个5天期间，食用10毫当量钠的饮食，并在双盲交叉研究中接受卡托普利（每日两次，每次25毫克）或安慰剂。
卡托普利降低了神经肽Y（p<0.05）和血管紧张素II（p<0.01），并增加了淋巴细胞中异丙肾上腺素刺激的环磷酸腺苷（AMP）（p<0.03）、血浆去甲肾上腺素（p<0.02）、皮质醇（p<0.05）和肾素（p<0.001），无论是高血压受试者还是血压正常受试者。与血压正常受试者相比，高血压受试者的β-肾上腺素能受体密度增加（p<0.02），舒张压下降幅度更大（p<0.02）。
本研究结果表明，卡托普利的短期治疗作用可能涉及交感神经系统关键成分的协同变化。这些发现，如神经肽Y减少与去甲肾上腺素和β-肾上腺素能受体增加相结合，与短期血管紧张素转换酶抑制后心输出量增加和外周阻力降低的观察结果一致。
