Evidence map›Paper›PMID 39542982›Full record

ArticleClinical autonomic research : official journal of the Clinical Autonomic Research Society2025

Sympathetic transduction to blood pressure in patients with chronic kidney disease.

Claire E Kissell, Benjamin E Young, Jasdeep Kaur, Ziba Taherzadeh, Ponnaiah C Mohan, Lauro C Vianna, Paul J Fadel

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Article in Clinical autonomic research : official journal of the Clinical Autonomic Research Society, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Claire E KissellDepartment of Kinesiology, University of Texas at Arlington, Arlington, TX, USA.
Benjamin E YoungDepartment of Kinesiology, Health Promotion and Recreation, University of North Texas, Denton, TX, USA.
Jasdeep KaurDepartment of Kinesiology and Health Education, University of Texas at Austin, Austin, TX, USA.
Ziba TaherzadehDepartment of Kinesiology, University of Texas at Arlington, Arlington, TX, USA.
Ponnaiah C MohanRenal Specialists of North Texas, Arlington, TX, USA.
Lauro C ViannaFaculty of Physical Education, University of Brasília, Brasília, DF, Brazil.
Paul J FadelDepartment of Kinesiology, University of Texas at Arlington, Arlington, TX, USA. paul.fadel@uta.edu.

Funding

Targeting Sympathetic Overactivity in CKD patients: Mechanisms & Novel TherapiesR01HL127071 · NHLBI · UNIVERSITY OF TEXAS ARLINGTON · PI FADEL, PAUL J · 2016 to 2019
$1.7M
NHLBI NIH HHS RO1 HL-127071
6 · The paper itself

Abstract

purposePatients 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.

methodsIn 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.

resultsPeak 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).

conclusionIn summary, these data indicate that patients with CKD do not have augmented sympathetic transduction to BP.

Indexed as

Blood PressureRenal Insufficiency, ChronicSympathetic Nervous SystemAdultAgedFemaleHumansMaleMiddle AgedMicroneurographyMuscle sympathetic nerve activityTotal vascular conductanceVasoconstriction

Identifiers

PMID39542982

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.