Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
J Appl Physiol (1985). 2013 Mar 1;114(5):538-49. doi: 10.1152/japplphysiol.01037.2012. Epub 2012 Dec 13.
Patients with chronic kidney disease (CKD) have poor exercise capacity, which contributes to cardiovascular risk. We sought to determine whether patients with stage 2 or stage 3 CKD have an augmented blood pressure (BP) response during exercise, and if so, whether overactivation of the sympathetic nervous system (SNS) during exercise might play a role. In 13 patients with CKD and hypertension and 13 controls with hypertension, we measured hemodynamics and muscle sympathetic nerve activity (MSNA) during the following maneuvers: low-level rhythmic handgrip (RHG 20%), which primarily stimulates mechanoreceptors, and moderate static handgrip exercise (SHG 30%) followed by posthandgrip circulatory arrest (PHGCA), which isolates metaboreceptors. During baseline studies, patients with CKD had significantly greater increases in mean arterial pressure (MAP) during SHG 30% (P = 0.045), RHG 20% (P = 0.031), and PHGCA (P = 0.043); however, the MSNA response was not augmented in patients with CKD compared with controls. We hypothesized that an augmented SNS response during exercise might be revealed in CKD if arterial baroreflex constraint was equalized using nitroprusside (NTP). These exercise maneuvers were repeated in patients with CKD during NTP infusion to equalize the BP response between groups, thereby relieving baroreflex-mediated suppression of SNS activity. With NTP infusion, patients with CKD had significantly increased MSNA responses during SHG 30% (P = 0.0044), and RHG 20% (P = 0.0064), but not during PHGCA (P > 0.05), suggesting increased reflex activation of the SNS during exercise, which may be mediated by mechanoreceptors but not metaboreceptors. Patients with CKD have an exaggerated BP response during rhythmic and static exercise with underlying SNS overactivation that is revealed during arterial baroreflex unloading during exercise.
患有慢性肾脏病 (CKD) 的患者运动能力较差，这会增加心血管风险。我们试图确定 2 期或 3 期 CKD 患者在运动期间是否会出现血压 (BP) 反应增强，如果是这样，运动期间交感神经系统 (SNS) 是否过度激活。在 13 名患有 CKD 和高血压的患者和 13 名患有高血压的对照组中，我们在以下操作期间测量了血流动力学和肌肉交感神经活动 (MSNA)：低水平节律性握力 (RHG 20% )，主要刺激机械感受器，以及中等强度的静态握力运动 (SHG 30%)，随后进行握力后循环阻断 (PHGCA)，以隔离代谢感受器。在基线研究中，CKD 患者在 SHG 30%（P = 0.045）、RHG 20%（P = 0.031）和 PHGCA（P = 0.043）期间的平均动脉压 (MAP) 升高显著增加；然而，与对照组相比，CKD 患者的 MSNA 反应并没有增强。我们假设，如果使用硝普钠 (NTP) 平衡动脉压力反射约束，CKD 患者在运动期间可能会出现 SNS 反应增强。在 NTP 输注期间，CKD 患者重复进行这些运动操作，以使两组之间的血压反应相等，从而减轻 SNS 活动的压力反射介导的抑制。在 NTP 输注期间，CKD 患者在 SHG 30%（P = 0.0044）和 RHG 20%（P = 0.0064）期间的 MSNA 反应显著增加，但在 PHGCA 期间没有增加（P > 0.05），这表明运动期间 SNS 的反射激活增加，这可能是由机械感受器介导的，但不是由代谢感受器介导的。CKD 患者在节律性和静态运动期间的血压反应增强，SNS 过度激活，在运动期间的动脉压力反射卸载期间显现。
