Publication

Nocturnal blood pressure is associated with sympathetic nerve activity in patients with chronic kidney disease

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Last modified
  • 05/15/2025
Type of Material
Authors
    Jin H. Jeong, Emory UniversityIda Fonkoue, Emory UniversityArshed Quyyumi, Emory UniversityDana DaCosta, Emory UniversityJeanie Park, Emory University
Language
  • English
Date
  • 2020-10-01
Publisher
  • Wiley Periodicals LLC
Publication Version
Copyright Statement
  • © 2020 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society
License
Final Published Version (URL)
Title of Journal or Parent Work
Volume
  • 8
Issue
  • 20
Start Page
  • e14602
End Page
  • e14602
Grant/Funding Information
  • This work was supported by the National Institutes of Health (NIH) R01 HL135183; NIH R61 AT10457; NIH Training Grant T32 DK00756; Merit Review Award number I01CX001065 from the United States Department of Veterans Affairs (VA) Clinical Sciences Research and Development Program; Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development and the Clinical Studies Center of the Atlanta VA Health Care System, Decatur, Georgia; and Foundation for Atlanta Veterans Education and Research (FAVER).
Abstract
  • Elevated nocturnal blood pressure (BP) and nocturnal non-dipping are frequently observed in patients with chronic kidney disease (CKD) and are stronger predictors of cardiovascular complications and CKD progression than standard office BP. The sympathetic nervous system (SNS) is thought to modulate diurnal hemodynamic changes and the vascular endothelium plays a fundamental role in BP regulation. We hypothesized that SNS overactivity and endothelial dysfunction in CKD are linked to elevated nocturnal BP and non-dipping. In 32 CKD patients with hypertension (56 ± 7 years), office BP, 24-hr ambulatory BP, muscle sympathetic nerve activity (MSNA) and endothelial function via flow-mediated dilation (FMD) were measured. Participants were subsequently divided into dippers (nighttime average BP > 10% lower than the daytime average BP, n = 8) and non-dippers (n = 24). Non-dippers had higher nighttime BP (p <.05), but not office and daytime BP, compared to dippers. MSNA burst incidence (81 ± 13 versus 67 ± 13 bursts/100 HR, p =.019) was higher and brachial artery FMD (1.7 ± 1.5 versus 4.7 ± 1.9%, p <.001) was lower in non-dippers compared to dippers. MSNA and FMD each predicted nighttime systolic (β = 0.48,-0.46, p =.02, 0.07, respectively) and diastolic BP (β = 0.38,-0.47, p =.04, 0.03, respectively) in multivariate-adjusted analyses. Our novel findings demonstrate that unfavorable nocturnal BP profiles are associated with elevated SNS activity and endothelial dysfunction in CKD. Specifically, CKD patients with higher nighttime BP and the non-dipping pattern have higher MSNA and lower FMD. These support our hypothesis that SNS overactivation and endothelial dysfunction are linked to the dysregulation of nighttime BP as well as the magnitude of BP lowering at nighttime in CKD.
Author Notes
  • Jeanie Park, Emory University /school of Medicine, 101 Woodruff Circle, Atlanta, GA 30322, USA; jeanie.park@emory.edu
Keywords
Research Categories
  • Health Sciences, Medicine and Surgery

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