Sympathetic Transduction to Blood Pressure in Patients with Chronic Kidney Disease

Abstract

Chronic kidney disease (CKD) is a major health problem affecting more than 35 million Americans. Notably, more patients with CKD die of cardiovascular complications than progress to end-stage renal disease. An overactive sympathetic nervous system is a well-known cardiovascular risk factor. Previous research has suggested elevated resting sympathetic nerve activity and a heightened α-adrenergic receptor sensitivity in patients with CKD, both of which may predispose this population to greater sympathetic transduction. Therefore, we tested the hypothesis that patients with stage III CKD have an augmented sympathetic transduction to blood pressure (BP) compared to controls without CKD. In 7 patients with stage III CKD and 8 controls muscle sympathetic nerve activity (MSNA; peroneal microneurography) and beat-to-beat BP (finometer) were continuously recorded during 10 minutes of quiet supine rest. Modelflow was used to estimate stroke volume and calculate total vascular conductance (TVC). Sympathetic transduction was quantified as the peak change in mean arterial pressure (MAP) and the nadir reduction of TVC over 10 cardiac cycles following spontaneous MSNA bursts using signal averaging. Patients with CKD and controls had similar resting MAP (CKD: 102 ± 14 mmHg; CON: 95 ± 8 mmHg; P = 0.27), MSNA burst frequency (CKD: 33 ± 10 bursts/min; CON: 31 ± 14 bursts/min; P = 0.78) and MSNA burst incidence (CKD: 53 ± 15 bursts/100 heartbeats; CON: 47 ± 24 bursts/100 heartbeats; P = 0.60). Peak increases in MAP following all bursts of MSNA were not different between patients with CKD and controls (CKD: 2.1 ± 0.7 mmHg; CON: 2.2 ± 0.9 mmHg; P = 0.83). Likewise, nadir reductions in TVC following all bursts of MSNA were not different in patients with CKD (CKD: -1.2 ± 0.6 ml/min/mmHg; CON: -1.4 ± 0.5 ml/min/mmHg; P = 0.46). Similar results were observed when considering burst patterning. MSNA bursts occurring in multiples (adjacent to other bursts) produced comparable peak MAP (CKD: 2.6 ± 0.6 mmHg; CON: 2.8 ± 1.2 mmHg; P = 0.67) and nadir TVC (CKD: -1.5 ± 0.7 ml/min/mmHg; CON: -1.9 ± 0.7 ml/min/mmHg; P = 0.25) responses between groups. There were also no differences in peak MAP and nadir TVC responses following single bursts of MSNA (bordered by cardiac cycles lacking bursts; both P > 0.30). These preliminary data suggest that, in contrast to our hypothesis, sympathetic transduction to BP is not augmented in patients with stage III CKD. This project was supported by the National Heart, Lung, and Blood Institute R01 HL-127071 (PJF). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.