Lund-Johansen P, Omvik P
Medical Department, Haukeland Hospital, University of Bergen, Norway.
Cardiovasc Drugs Ther. 1991 Jun;5(3):605-15. doi: 10.1007/BF03029729.
The regulation of vascular resistance, cardiac output, and thus blood pressure can be influenced by antihypertensive drugs acting at central and peripheral adrenergic receptors. The results presented here are from acute or chronic studies in 205 patients with mild or moderately severe essential hypertension: beta blockers (N = 101); alpha blockers (N = 36); a separate alpha- + beta-blocker combination or the combination agent labetalol (N = 37); prizidilol, a beta-blocker/vasodilator (N = 14); and dilevalol, a beta blocker/beta 2-stimulator (N = 17). Beta blockers without strong intrinsic sympathomimetic activity reduce heart rate and cardiac output immediately, but due to a reflex increase in total peripheral resistance index, blood pressure is unchanged or only slightly reduced. During chronic use, total peripheral resistance drops towards pretreatment level and pressure falls. Beta blockers with strong intrinsic sympathomimetic activity do not reduce heart rate or cardiac output at rest when sympathetic tone is low. During exercise, heart rate and cardiac output are reduced, but less than with conventional beta blockers, and resistance is unchanged or slightly reduced. An acute and chronic reduction in blood pressure can be produced by alpha-adrenergic receptor blockers (prazosin, doxazosin, trimazosin), and in these cases the fall occurs via a reduction in total peripheral resistance index without reflex tachycardia. These drugs tend to increase exercise stroke volume and cardiac output during chronic treatment. Free combinations of beta and alpha blockers or the use of the fixed combination drug, labetalol, induce marked reductions in blood pressure at rest and during exercise, mainly through a reduction in total peripheral resistance index. During chronic treatment, exercise stroke volume and cardiac output are well maintained. In acute studies with dilevalol, systolic blood pressure, diastolic blood pressure, and mean arterial pressure were reduced (p less than 0.001) within 1 hour in 17 males with essential hypertension (WHO stage I) who received 200-400 mg oral dilevalol. The reduction in MAP was around 16-17% and was associated with an immediate fall in the total peripheral resistance index of the same magnitude (14%, p less than 0.001) after 1 hour at rest. There were no significant changes in heart rate or cardiac index.(ABSTRACT TRUNCATED AT 400 WORDS)
作用于中枢和外周肾上腺素能受体的抗高血压药物可影响血管阻力、心输出量,进而影响血压。本文给出的结果来自对205例轻度或中度重度原发性高血压患者进行的急性或慢性研究:β受体阻滞剂(N = 101);α受体阻滞剂(N = 36);单独的α + β受体阻滞剂联合用药或联合制剂拉贝洛尔(N = 37);β受体阻滞剂/血管扩张剂普齐地洛(N = 14);以及β受体阻滞剂/β2激动剂地来洛尔(N = 17)。无强大内在拟交感活性的β受体阻滞剂可立即降低心率和心输出量,但由于总外周阻力指数反射性增加,血压不变或仅略有降低。在长期使用期间,总外周阻力降至治疗前水平,血压下降。具有强大内在拟交感活性的β受体阻滞剂在交感神经张力较低时,静息状态下不会降低心率或心输出量。在运动期间,心率和心输出量会降低,但降幅小于传统β受体阻滞剂,且阻力不变或略有降低。α肾上腺素能受体阻滞剂(哌唑嗪、多沙唑嗪、曲马唑嗪)可产生急性和慢性血压降低,在这些情况下,血压下降是通过降低总外周阻力指数实现的,且无反射性心动过速。在长期治疗期间,这些药物往往会增加运动时的每搏输出量和心输出量。β受体阻滞剂和α受体阻滞剂的自由联合用药或使用固定复方制剂拉贝洛尔,可使静息和运动时的血压显著降低,主要是通过降低总外周阻力指数实现的。在长期治疗期间,运动时的每搏输出量和心输出量能得到良好维持。在地来洛尔的急性研究中,17例患有原发性高血压(WHO I期)的男性口服200 - 400 mg地来洛尔后,1小时内收缩压、舒张压和平均动脉压均降低(p < 0.001)。平均动脉压降低约16 - 17%,且与静息1小时后总外周阻力指数立即下降相同幅度(14%,p < 0.001)相关。心率或心脏指数无显著变化。(摘要截选至400字)