Schmieder R E, Rüddel H, Schächinger H, Bruns J, Schulte W
Department of Medicine, University of Bonn, Federal Republic of Germany.
Behav Med. 1993 Spring;19(1):5-12. doi: 10.1080/08964289.1993.9937558.
To examine whether sympathetic nervous activation has an impact on renal circulation in subjects at risk for high blood pressure, we assessed renal hemodynamics and cardiovascular response to mental stress in 40 healthy young white males, 12 normotensive subjects without and 14 with familial hypertension, and 14 with borderline hypertension. The response of systolic and diastolic blood pressure to mental stress was assessed while each patient performed a mental arithmetic task; this was taken as the parameter for the activation of the sympathetic nervous system. Renal plasma flow was measured by para-aminohippuric acid clearance under steady-state conditions. In parallel, glomerular filtration rate as a parameter for functional impairment of the kidneys was determined by creatinine clearance, and filtration fraction was also calculated. Patients with borderline hypertension were characterized by a reduced renal blood flow and increased filtration fraction in comparison with both normotensive groups. The increase in systolic blood pressure during mental stress was more pronounced in borderline hypertensives. We observed no significant difference in renal hemodynamics and cardiovascular response to mental stress between normotensives with and without a family history of hypertension. In the total population, cardiovascular response to mental stress was correlated with renal hemodynamics: The greater the increase in systolic blood pressure during mental stress, the lower was the renal plasma flow and the greater the filtration fraction. Thus, renal plasma flow was found to be already reduced and filtration fraction increased before sustained hypertension developed. Because this pattern in renal hemodynamics was related to cardiovascular response to mental stress, our data suggest that sympathetic activation already appeared to affect renal hemodynamics at the onset of essential hypertension.
为了研究交感神经激活是否对有高血压风险的受试者的肾循环有影响,我们评估了40名健康年轻白人男性、12名无家族高血压病史的血压正常受试者、14名有家族性高血压的血压正常受试者以及14名临界高血压患者的肾脏血流动力学和对精神应激的心血管反应。在每位患者进行心算任务时评估收缩压和舒张压对精神应激的反应;这被用作交感神经系统激活的参数。在稳态条件下通过对氨基马尿酸清除率测量肾血浆流量。同时,通过肌酐清除率测定肾小球滤过率作为肾脏功能损害的参数,并计算滤过分数。与两个血压正常组相比,临界高血压患者的特点是肾血流量减少和滤过分数增加。临界高血压患者在精神应激期间收缩压的升高更为明显。我们观察到有高血压家族史和无高血压家族史的血压正常受试者在肾脏血流动力学和对精神应激的心血管反应方面没有显著差异。在总体人群中,对精神应激的心血管反应与肾脏血流动力学相关:精神应激期间收缩压升高越大,肾血浆流量越低,滤过分数越高。因此,在持续性高血压发展之前,肾血浆流量就已降低,滤过分数增加。由于这种肾脏血流动力学模式与对精神应激的心血管反应有关,我们的数据表明交感神经激活在原发性高血压发病时似乎已经影响肾脏血流动力学。