Heaney A P, Hunter S J, Sheridan B, Brew Atkinson A
Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Belfast, UK.
Clin Endocrinol (Oxf). 1999 Sep;51(3):293-9. doi: 10.1046/j.1365-2265.1999.00766.x.
The mechanism of hypertension in Cushing's syndrome remains undetermined. Some studies have demonstrated an increased sensitivity to pressor agents but it is not clear if patients with Cushing's syndrome of different aetiologies demonstrate this finding. We have examined pressor sensitivity in a group of patients with Cushing's disease (pituitary dependent hypercortisolism) by measuring blood pressure during incrementally increasing infusions of noradrenaline.
Eight subjects (7 female, 1 male), aged 42.2 +/- 4.5 years (mean +/- SEM) with Cushing's disease were studied. Eight age- and sex-matched control subjects were also studied. Four of the eight controls and five patients with Cushing's disease had elevated blood pressure. All medication for this had been stopped at least seven days prior to the study. After subjects ate a light breakfast, ECG leads and a sphygmomanometer were attached, an intravenous cannula was inserted and all subjects then rested quietly for 60 minutes. Noradrenaline was then infused intravenously for 10-minute periods at concentrations of 0.01, 0.03, 0.07, 0.11 and 0.18 microg/kg/minute.
On the day of the study the baseline blood pressures and pulse rates in the patients with Cushing's disease (blood pressure; 138/87 +/- 6/3 mmHg, pulse 76.5 +/- 4.8 beats/minute) and controls (blood pressure; 126/86 +/- 6/6 mmHg, pulse 71.2 +/- 3.7 beats/minute) were not significantly different. The mean change in diastolic blood pressure from baseline at the time of the peak increase or when the test was stopped was 21. 5 +/- 4.7 mmHg in Cushing's disease compared to 7.0 +/- 2.5 mmHg in controls (P = 0.03). The mean change in mean arterial pressure from baseline at the time of the peak increase or when the test was stopped was 22.0 +/- 4.0 mmHg in Cushing's disease compared to 13.0 +/- 2.4 mmHg in controls (P = 0.03). No significant difference in mean change of systolic pressure (26.0 +/- 4.6 vs. 25 +/- 4.0 mmHg) or pulse rates (- 11.1 +/- 1.8 vs. - 4.7 +/- 2.6) was seen in the group with Cushing's disease as compared to the control group.
We conclude that patients with pituitary-dependent Cushing's syndrome have enhanced pressor diastolic and mean arterial responses to noradrenaline and this may be an important underlying mechanism for the hypertension seen in this particular group of Cushing's syndrome patients.
库欣综合征中高血压的机制仍未明确。一些研究表明对升压药的敏感性增加，但不同病因的库欣综合征患者是否有此表现尚不清楚。我们通过在递增输注去甲肾上腺素期间测量血压，研究了一组库欣病（垂体依赖性皮质醇增多症）患者的升压敏感性。
研究了8名年龄在42.2±4.5岁（平均±标准误）的库欣病患者（7名女性，1名男性）。还研究了8名年龄和性别匹配的对照者。8名对照者中的4名和5名库欣病患者血压升高。在研究前至少7天已停用所有相关药物。受试者吃了清淡早餐后，连接心电图导联和血压计，插入静脉套管，然后所有受试者安静休息60分钟。然后以0.01、0.03、0.07、0.11和0.18微克/千克/分钟的浓度静脉输注去甲肾上腺素10分钟。
在研究当天，库欣病患者（血压：138/87±6/3 mmHg，脉搏76.5±4.8次/分钟）和对照者（血压：126/86±6/6 mmHg，脉搏71.2±3.7次/分钟）的基线血压和脉搏率无显著差异。库欣病患者在升压峰值时或试验停止时舒张压相对于基线的平均变化为21.5±4.7 mmHg，而对照者为7.0±2.5 mmHg（P = 0.03）。库欣病患者在升压峰值时或试验停止时平均动脉压相对于基线的平均变化为22.0±4.0 mmHg，而对照者为13.0±2.4 mmHg（P = 0.03）。与对照组相比，库欣病组收缩压平均变化（26.0±4.6对25±4.0 mmHg）或脉搏率（-11.1±1.8对-4.7±2.6）无显著差异。
我们得出结论，垂体依赖性库欣综合征患者对去甲肾上腺素的舒张压和平均动脉压升压反应增强，这可能是该特定组库欣综合征患者出现高血压的重要潜在机制。
