Park Jeanie, Middlekauff Holly R
Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA; Research Service Line, Department of Veterans Affairs Medical Center, Decatur, GA, USA.
Cardiology Division, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Auton Neurosci. 2015 Mar;188:74-81. doi: 10.1016/j.autneu.2014.10.013. Epub 2014 Oct 22.
Abnormal neurocirculatory control during exercise is one important mechanism leading to exercise intolerance in patients with both end-stage renal disease (ESRD) and earlier stages of chronic kidney disease (CKD). This review will provide an overview of mechanisms underlying abnormal neurocirculatory and hemodynamic responses to exercise in patients with kidney disease. Recent studies have shown that ESRD and CKD patients have an exaggerated increase in blood pressure (BP) during both isometric and rhythmic exercise. Subsequent studies examining the role of the exercise pressor reflex in the augmented pressor response revealed that muscle sympathetic nerve activity (MSNA) was not augmented during exercise in these patients, and metaboreflex-mediated increases in MSNA were blunted, while mechanoreflex-mediated increases were preserved under basal conditions. However, normalizing the augmented BP response during exercise via infusion of nitroprusside (NTP), and thereby equalizing baroreflex-mediated suppression of MSNA, an important modulator of the final hemodynamic response to exercise, revealed that CKD patients had an exaggerated increase in MSNA during isometric and rhythmic exercise. In addition, mechanoreflex-mediated control was augmented, and metaboreceptor blunting was no longer apparent in CKD patients with baroreflex normalization. Factors leading to mechanoreceptor sensitization, and other mechanisms underlying the exaggerated exercise pressor response, such as impaired functional sympatholysis, should be investigated in future studies.
运动期间神经循环控制异常是导致终末期肾病（ESRD）和慢性肾病（CKD）早期患者运动不耐受的一个重要机制。本综述将概述肾病患者运动时神经循环和血流动力学异常反应的潜在机制。最近的研究表明，ESRD和CKD患者在等长运动和节律性运动期间血压（BP）过度升高。随后研究运动升压反射在增强的升压反应中的作用发现，这些患者运动期间肌肉交感神经活动（MSNA）并未增强，且代谢反射介导的MSNA增加减弱，而在基础条件下机械反射介导的增加得以保留。然而，通过输注硝普钠（NTP）使运动期间增强的BP反应正常化，从而使压力反射介导的MSNA抑制作用均衡（MSNA是运动最终血流动力学反应的重要调节因子），结果显示CKD患者在等长运动和节律性运动期间MSNA过度增加。此外，在压力反射正常化的CKD患者中，机械反射介导的控制增强，代谢感受器钝化不再明显。未来研究应探讨导致机械感受器敏感化的因素以及运动升压反应过度的其他机制，如功能性交感神经抑制受损。
