Guerrero Rosa V D, Vianna Lauro C, Lehnen Georgia C S, Daher Mauricio, Teixeira André L, Fernandes Igor A
NeuroV̇ASQ̇-Integrative Physiology Laboratory, Faculty of Physical Education, University of Brasília, Brasília, DF, Brazil.
School of Exercise and Nutrition Sciences, Faculty of Health, Queensland University of Technology, Brisbane, QLD, Australia.
Clin Auton Res. 2025 Apr;35(2):277-284. doi: 10.1007/s10286-024-01105-5. Epub 2025 Jan 15.
Resting beat-to-beat blood pressure variability is a strong predictor of cardiovascular events and mortality. However, its underlying mechanisms remain incompletely understood. Given that the sympathetic nervous system plays a pivotal role in cardiovascular regulation, we hypothesized that alpha-1 adrenergic receptors (the main sympathetic receptor controlling peripheral vasoconstriction) may contribute to resting beat-to-beat blood pressure variability.
Beat-to-beat heart rate (electrocardiography) and blood pressure (photoplethysmography) were continuously measured before and 2 h following, selective blockade of alpha-1 adrenergic receptors via oral administration of prazosin (1 mg/20 kg) in ten young healthy adults (two women). Cardiac output and total peripheral resistance were estimated using the ModelFlow method.
Selective blockade of alpha-1 adrenergic receptors was confirmed by the marked reduction in the pressor response to intravenous infusion of phenylephrine hydrochloride (-80 ± 15%, P = 0.001 versus pre-prazosin). The blockade significantly decreased the standard deviation of the systolic (pre-prazosin versus post-prazosin: 5.6 ± 1.4 versus 3.8 ± 0.7 mmHg, P = 0.002), diastolic (3.2 ± 1.2 versus 2.2 ± 0.5 mmHg, P = 0.022), and mean blood pressure (3.7 ± 1.2 versus 2.5 ± 0.5 mmHg, P = 0.009), as well as total peripheral resistance (0.8 ± 0.5 versus 0.5 ± 0.1 mmHg/L/min, P = 0.047), but not cardiac output (521 ± 188 versus 453 ± 160 mL/min, P = 0.321). Similar results were found using different indices of variability.
These findings indicate that alpha-1 adrenergic receptors play a significant role in regulating resting beat-to-beat blood pressure variability in young, healthy adults.
静息状态下逐搏血压变异性是心血管事件和死亡率的有力预测指标。然而,其潜在机制仍未完全明确。鉴于交感神经系统在心血管调节中起关键作用,我们推测α-1肾上腺素能受体(控制外周血管收缩的主要交感神经受体)可能与静息状态下逐搏血压变异性有关。
对10名年轻健康成年人(2名女性)口服哌唑嗪(1毫克/20千克)选择性阻断α-1肾上腺素能受体,在给药前及给药后2小时连续测量逐搏心率(心电图)和血压(光电容积脉搏波描记法)。采用ModelFlow方法估算心输出量和总外周阻力。
静脉注射盐酸去氧肾上腺素后升压反应显著降低,证实了α-1肾上腺素能受体被选择性阻断(与哌唑嗪给药前相比,降低了-80±15%,P = 0.001)。阻断后,收缩压(哌唑嗪给药前与给药后:5.6±1.4与3.8±0.7毫米汞柱,P = 0.002)、舒张压(3.2±1.2与2.2±0.5毫米汞柱,P = 0.022)和平均血压(3.7±1.2与2.5±0.5毫米汞柱,P = 0.009)的标准差以及总外周阻力(0.8±0.5与0.5±0.1毫米汞柱/升/分钟,P = 0.047)均显著降低,但心输出量未降低(521±188与453±160毫升/分钟,P = 0.321)。使用不同的变异性指标也得到了类似结果。
这些发现表明,α-1肾上腺素能受体在调节年轻健康成年人静息状态下逐搏血压变异性方面起重要作用。