Kissell Claire E, Young Benjamin E, Kaur Jasdeep, Taherzadeh Ziba, Mohan Ponnaiah C, Vianna Lauro C, Fadel Paul J
Department of Kinesiology, University of Texas at Arlington, Arlington, TX, USA.
Department of Kinesiology, Health Promotion and Recreation, University of North Texas, Denton, TX, USA.
Clin Auton Res. 2025 Apr;35(2):223-230. doi: 10.1007/s10286-024-01084-7. Epub 2024 Nov 14.
Patients with chronic kidney disease (CKD) are more than twice as likely to die from a cardiovascular event than those with normal kidney function. Although CKD may increase resting sympathetic activity, quantification of resting sympathetic outflow alone does not account for the ensuing vasoconstriction, and blood pressure (BP) change (i.e., sympathetic transduction). Patients with CKD have been reported to exhibit elevated α-adrenergic receptor sensitivity, which may predispose this population to greater sympathetic transduction. We tested the hypothesis that patients with CKD have augmented sympathetic transduction to BP.
In 16 patients with CKD, 17 bodyweight-matched (BWM) controls, and 11 lean controls of a similar age muscle sympathetic nerve activity (MSNA) and beat-to-beat BP were continuously recorded during quiet supine rest. Signal averaging was used to quantify changes in mean arterial pressure (MAP) and total vascular conductance (TVC) following spontaneous bursts of MSNA.
Peak increases in MAP following MSNA bursts were not different among patients with CKD and the control groups (CKD: 2.3 ± 1.1 mmHg; BWM controls: 2.1 ± 1.0 mmHg; lean controls: 1.7 ± 0.9 mmHg; P = 0.28). Likewise, nadir reductions in TVC following all bursts of MSNA were not different among patients with CKD and either control group (P = 0.69). Both patients with CKD and controls had graded increases in MAP and decreases in TVC with increasing burst size, which were not different among groups (all P > 0.05).
In summary, these data indicate that patients with CKD do not have augmented sympathetic transduction to BP.
慢性肾脏病（CKD）患者死于心血管事件的可能性是肾功能正常者的两倍多。虽然CKD可能会增加静息交感神经活动，但仅对静息交感神经输出进行量化并不能解释随之而来的血管收缩以及血压（BP）变化（即交感神经传导）。据报道，CKD患者表现出α-肾上腺素能受体敏感性升高，这可能使该人群更容易发生交感神经传导。我们检验了CKD患者交感神经向血压的传导增强这一假设。
对16例CKD患者、17例体重匹配（BWM）的对照者以及11例年龄相仿的瘦对照者在安静仰卧休息期间连续记录肌肉交感神经活动（MSNA）和逐搏血压。信号平均用于量化MSNA自发爆发后平均动脉压（MAP）和总血管传导（TVC）的变化。
CKD患者和对照组在MSNA爆发后MAP的峰值增加没有差异（CKD：2.3±1.1 mmHg；BWM对照：2.1±1.0 mmHg；瘦对照：1.7±0.9 mmHg；P = 0.28）。同样，在所有MSNA爆发后TVC的最低点降低在CKD患者和任一对照组之间也没有差异（P = 0.69）。CKD患者和对照组的MAP均随爆发大小增加而分级升高，TVC则降低，各组之间没有差异（所有P>0.05）。
总之，这些数据表明CKD患者交感神经向血压的传导没有增强。
