Effects of nifedipine on baroreflex modulation of vascular resistance in man.
Effects of nifedipine on baroreflex modulation of vascular resistance in man.
复制标题
硝苯地平对人体血管阻力压力反射调节的影响。
DOI：
10.1016/0002-8703(85)90415-6
复制
发表时间：
1985
影响因子：
4.8
通讯作者：
Dorsey,JK
中科院分区：
文献类型：
--
作者：
Ferguson,DW;Dorsey,JK
动物研究表明，除了对血管的影响外，钙通道阻滞剂对压力感受器功能也有重要影响。我们进行了一系列的实验，以确定是否硝苯地平，在临床上使用的剂量，改变压力反射控制血管阻力在正常人。本文观察了14名正常人前臂对下体负压（LBNP）压力感受器卸荷、冷加压试验和动脉灌注去甲肾上腺素时的收缩反应。硝苯地平对基线平均动脉压或中心静脉压无影响。硝苯地平治疗后心率和前臂血流量显著增加：治疗前心率为59.7 ± 2.4次/分，治疗后为72.6 ± 4.4次/分硝苯地平治疗前FBF = 4.6 ± 0.4 ml·min-1·100 ml-1，治疗后FBF = 6.7 ± 1.0 ml·min-1·100 ml-1（p <0.02，n = 14）。硝苯地平给药后前臂血管阻力（FVR）趋于降低，但差异不显著：硝苯地平给药前FVR = 21.1 ± 1.4单位，给药后FVR = 17.8 ± 2.3单位（p = 0.07，n = 14）。硝苯地平减弱冷加压刺激引起的前臂血管收缩反应：冷加压试验中硝苯地平给药前和给药后的Δ FVR分别为+10.3 ± 2.4和+4.7 ± 1.4单位（p <0.02，n = 14）。同样，硝苯地平抑制了动脉内输注去甲肾上腺素的血管收缩反应：去甲肾上腺素期间的Δ FVR =硝苯地平前+15.5 ± 3.4单位，硝苯地平后+10.2 ± 2.9单位（p <0.05，n = 7）。与此相反，硝苯地平没有改变LBNP压力感受器卸载的血管收缩反应：LBNP − 10 mm Hg期间的Δ FVR =用药前+4.8 ± 1.7单位，用药后+4.1 ± 1.1单位（p = NS，n = 14）;硝苯地平给药前和给药后LBNP − 40 mmHg期间的Δ FVR分别为+15.0 ± 2.1单位和+15.6 ± 3.0单位（p = NS，n = 14）。尽管血管反应性降低，但压力感受性反射反应仍得以保留，这一发现表明硝苯地平可使正常人的压力感受性反射敏感。治疗剂量硝苯地平后的这些效应可能对该药物的治疗用途有影响。
Studies in animals have demonstrated that, in addition to their vascular effects, calcium channel blockers have important effects on baroreceptor function. We performed a series of experiments to determine if nifedipine, in doses employed clinically, alters baroreflex control of vascular resistance in normal humans. Forearm vasoconstrictor responses of 14 normal subjects to unloading of baroreceptors with lower body negative pressure (LBNP), to a cold pressor test and during intra-arterial infusions of norepinephrine were studied in the control state and following administration of nifedipine. Nifedipine had no effect on baseline mean arterial pressure or central venous pressure. Heart rate and forearm blood flow (FBF) increased significantly following nifedipine: heart rate = 59.7 ± 2.4 bpm before and 72.6 ± 4.4 bpm after nifedipine (mean ± SE,p< 0.001, n = 14); FBF = 4.6 ± 0.4 ml · min−1· 100 ml−1before and 6.7 ± 1.0 ml · min1· 100 ml−1after nifedipine (p< 0.02, n = 14). Forearm vascular resistance (FVR) tended to decrease following nifedipine but the difference was not significant: FVR = 21.1 ± 1.4 units before and 17.8 ± 2.3 units after nifedipine (p= 0.07, n = 14). Nifedipine attenuated forearm vasoconstrictor responses to cold pressor stimulus: ΔFVR during cold pressor test = +10.3 ± 2.4 units before and +4.7 ± 1.4 units after nifedipine (p< 0.02, n = 14). Likewise, nifedipine depressed vasoconstrictor responses to intra-arterial infusion of norepinephrine: ΔFVR during norepinephrine = +15.5 ± 3.4 units before and +10.2 ± 2.9 units after nifedipine (p< 0.05, n = 7). In contrast, the vasoconstrictor responses to unloading of baroreceptors with LBNP were not altered by nifedipine: ΔFVR during LBNP −10 mm Hg = +4.8 ± 1.7 units before and +4.1 ± 1.1 units after the drug (p= NS, n = 14); ΔFVR during LBNP −40 mm Hg = +15.0 ± 2.1 units before and +15.6 ± 3.0 units after nifedipine (p= NS, n = 14). The finding that baroreflex responses were preserved despite a decrease in vascular responsiveness suggests that nifedipine sensitizes baroreflexes in normal humans. These effects following a therapeutic dose of nifedipine may have implications in the therapeutic use of this agent.