Stewart Kerry J, Sung Jidong, Silber Harry A, Fleg Jerome L, Kelemen Mark D, Turner Katherine L, Bacher Anita C, Dobrosielski Devon A, DeRegis James R, Shapiro Edward P, Ouyang Pamela
Department of Medicine, Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, Maryland 21224, USA.
Am J Hypertens. 2004 Apr;17(4):314-20. doi: 10.1016/S0895-7061(03)01003-3.
Persons with high normal blood pressure (BP) or mild hypertension who also have an exaggerated BP response to exercise are at risk for worsening hypertension. The mechanisms that explain this relationship are unknown. We examined the relationships of endothelial vasodilator function and of aortic stiffness with exercise BP.
Subjects were 38 men and 44 women, aged 55 to 75 years, with untreated high normal BP or mild hypertension but otherwise healthy. Exercise was performed on a treadmill. Endothelial vasodilator function was assessed as brachial artery flow-mediated vasodilation (FMD) during reactive hyperemia. Aortic stiffness was measured as pulse wave velocity (PWV).
Among men, resting systolic BP explained 34% of the variance (P < .01) in maximal exercise systolic BP and FMD explained an additional 11% (P < .01); resting systolic BP explained 23% of the variance in maximal pulse pressure (PP) (P < .01), and FMD explained an additional 10% (P < .01). Among women, resting systolic BP was the only independent correlate of maximal systolic BP (R2 = 0.12, P < .03) and FMD correlated negatively with maximal PP (R2 = 0.12, P < .03). Among men, FMD was the only independent correlate of the difference between resting and maximal systolic BP (R2 = 0.20, P < .02). The FMD was the only independent correlate of the difference between resting and maximal PP among men (R2 = 0.17, P < .03) and among women (R2 = 0.12, P < .03). The PWV did not correlate with exercise BP responses.
These results suggest that impaired endothelial vasodilator function may be a mechanism contributing to exercise hypertension and may also be one link between exaggerated exercise BP and worsening hypertension.
血压处于正常高值或患有轻度高血压且运动时血压反应过度的人，有高血压病情恶化的风险。解释这种关系的机制尚不清楚。我们研究了内皮舒张功能和主动脉僵硬度与运动血压之间的关系。
研究对象为38名男性和44名女性，年龄在55至75岁之间，未经治疗的血压处于正常高值或患有轻度高血压，但其他方面健康。在跑步机上进行运动。内皮舒张功能通过反应性充血期间肱动脉血流介导的血管舒张（FMD）进行评估。主动脉僵硬度通过脉搏波速度（PWV）测量。
在男性中，静息收缩压解释了最大运动收缩压变异的34%（P <.01），FMD额外解释了11%（P <.01）；静息收缩压解释了最大脉压（PP）变异的23%（P <.01），FMD额外解释了10%（P <.01）。在女性中，静息收缩压是最大收缩压的唯一独立相关因素（R2 = 0.12，P <.03），FMD与最大PP呈负相关（R2 = 0.12，P <.03）。在男性中，FMD是静息和最大收缩压差值的唯一独立相关因素（R2 = 0.20，P <.02）。FMD是男性（R2 = 0.17，P <.03）和女性（R2 = 0.12，P <.03）静息和最大PP差值的唯一独立相关因素。PWV与运动血压反应无关。
这些结果表明，内皮舒张功能受损可能是导致运动性高血压的一种机制，也可能是运动血压过度与高血压病情恶化之间的一个联系。
