Macefield V G, Williamson P M, Wilson L R, Kelly J J, Gandevia S C, Whitworth J A
Prince of Wales Medical Research Institute, Randwick, Australia.
Blood Press. 1998 Jul;7(4):215-22. doi: 10.1080/080370598437240.
This study was undertaken to test the hypothesis that increased sympathetic vasomotor drive is responsible for cortisol-induced hypertension.
Ten healthy male subjects on a fixed sodium diet (150 mmol/day) were randomized to five days of treatment with cortisol (200 mg/day) or placebo in a double-blind crossover study. On day 5 of each treatment, multi-unit muscle sympathetic activity was recorded from the common peroneal nerve. Resting muscle sympathetic activity (MSA) was measured in the recumbent position and stimulated MSA was measured in the final 20 sec of end-inspiratory capacity apnoea and end-expiratory apnoea and in the second minute of a cold pressor stimulus. A subgroup of six subjects also underwent identical MSA measurements following 5 days treatment with dexamethasone (3 mg/day).
Cortisol, but not placebo, significantly increased systolic (115+/-2 vs 129+/-3 mmHg precortisol vs cortisol day 5, p < 0.001) and diastolic blood pressure (53+/-3 vs 61+/-3, p < 0.05). Resting MSA was significantly reduced by cortisol (23.9+/-2.3 to 5.0+/-2.0 bursts/min, placebo vs cortisol, p < 0.01). Cortisol significantly attenuated the increase in MSA observed at end-inspiratory apnoea (56.3+/-3.9 vs 35.4+/-6.6, p < 0.05) and end-expiratory apnoea (50.5+/-3.5 vs 26.3+/-6.2 bursts/min, n = 8, p < 0.05), and during the cold pressor response (55.0+/-12.7 vs 21.4+/-7.6, n = 5, p < 0.05). Dexamethasone significantly increased systolic blood pressure and suppressed resting and stimulated MSA. No changes in body weight, haematocrit or angiotensin II concentrations occurred during dexamethasone treatment.
MSA is significantly suppressed by cortisol treatment. As suppression of MSA is also observed during treatment with the pure glucocorticoid dexamethasone, suppressed MSA cannot be attributed to increased plasma volume or to changes in angiotensin II concentration. We conclude that cortisol-induced hypertension is not due to increased muscle sympathetic vasomotor drive.
本研究旨在验证交感缩血管驱动力增加是皮质醇诱导高血压的原因这一假说。
在一项双盲交叉研究中，10名遵循固定钠饮食（150毫摩尔/天）的健康男性受试者被随机分为两组，分别接受为期5天的皮质醇（200毫克/天）或安慰剂治疗。在每种治疗的第5天，从腓总神经记录多单位肌肉交感神经活动。在卧位测量静息肌肉交感神经活动（MSA），并在吸气末屏气和呼气末屏气的最后20秒以及冷加压刺激的第二分钟测量刺激后的MSA。6名受试者的亚组在接受地塞米松（3毫克/天）治疗5天后也进行了相同的MSA测量。
皮质醇而非安慰剂显著升高收缩压（皮质醇治疗前为115±2毫米汞柱，第5天为129±3毫米汞柱，p<0.001）和舒张压（53±3毫米汞柱 vs 61±3毫米汞柱，p<0.05）。皮质醇使静息MSA显著降低（安慰剂组为23.9±2.3次/分钟，皮质醇组为5.0±2.0次/分钟，p<0.01）。皮质醇显著减弱了吸气末屏气（56.3±3.9次/分钟 vs 35.4±6.6次/分钟，p<0.05）和呼气末屏气（50.5±3.5次/分钟 vs 26.3±6.2次/分钟，n = 8，p<0.05）以及冷加压反应期间（55.0±12.7次/分钟 vs 21.4±7.6次/分钟，n = 5，p<0.05）观察到的MSA增加。地塞米松显著升高收缩压并抑制静息和刺激后的MSA。在地塞米松治疗期间，体重、血细胞比容或血管紧张素II浓度没有变化。
皮质醇治疗可显著抑制MSA。由于在使用纯糖皮质激素地塞米松治疗期间也观察到MSA受到抑制，因此MSA受到抑制不能归因于血浆量增加或血管紧张素II浓度的变化。我们得出结论，皮质醇诱导的高血压并非由于肌肉交感缩血管驱动力增加所致。
