Stadeager C, Hesse B, Henriksen O, Christensen N J, Bonde-Petersen F, Mehlsen J, Giese J
Department of Clinical Physiology, Hvidovre Hospital, Copenhagen, Denmark.
J Appl Physiol (1985). 1989 Aug;67(2):786-91. doi: 10.1152/jappl.1989.67.2.786.
The effects of angiotensin-converting enzyme inhibition (ACE-I) by enalapril on splanchnic (n = 10) and central hemodynamics (n = 9) were examined in moderately salt-depleted healthy volunteers, at rest and during 15-20 min of lower body negative pressure (LBNP), reducing mean arterial pressure by 10 mmHg. During LBNP before ACE-I, both splanchnic and total peripheral vascular resistances increased. During ACE-I, splanchnic and total peripheral vascular resistances decreased. After enalapril administration, splanchnic vascular resistance did not increase during LBNP. Total peripheral vascular resistance still increased but not to the same extent as during LBNP before ACE-I. The increases in heart rate and plasma norepinephrine during LBNP were attenuated after ACE-I compared with LBNP before ACE-I. The effectiveness of the ACE-I was clearly demonstrated by unchanged and low plasma angiotensin II levels during ACE-I. We conclude that, in normal sodium-depleted humans, acute ACE-I decreases splanchnic vascular resistance at rest and abolishes splanchnic vasoconstriction during LBNP. Furthermore, it may interfere with autonomic nervous system control of the circulation.
在轻度缺盐的健康志愿者中，研究了依那普利对内脏（n = 10）和中心血流动力学（n = 9）的血管紧张素转换酶抑制（ACE-I）作用，分别于静息状态以及在下肢负压（LBNP）15 - 20分钟期间进行观察，LBNP使平均动脉压降低10 mmHg。在ACE-I治疗前的LBNP期间，内脏和总外周血管阻力均增加。在ACE-I治疗期间，内脏和总外周血管阻力降低。给予依那普利后，LBNP期间内脏血管阻力未增加。总外周血管阻力仍有增加，但程度不如ACE-I治疗前的LBNP期间。与ACE-I治疗前的LBNP相比，ACE-I治疗后LBNP期间心率和血浆去甲肾上腺素的增加有所减弱。ACE-I治疗期间血浆血管紧张素II水平保持不变且较低，清楚地证明了ACE-I的有效性。我们得出结论，在正常缺钠的人体中，急性ACE-I可降低静息时的内脏血管阻力，并消除LBNP期间的内脏血管收缩。此外，它可能会干扰自主神经系统对循环的控制。
