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Unaltered neurocardiovascular reactions to mental stress after renal sympathetic denervation

Journal article
Authors Sebastian Völz
Linda Lundblad
Bert Andersson
Jonas Multing
Bengt Rundqvist
Mikael Elam
Published in Clinical and Experimental Hypertension
Volume 42
Issue 2
Pages 160-166
ISSN 1064-1963
Publication year 2020
Published at Institute of Neuroscience and Physiology
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 160-166
Language en
Links dx.doi.org/10.1080/10641963.2019.15...
Keywords Renal hypertension, multi-unit muscle sympathetic nerve activity, renal, denervation, sympathectomy, arousal, physiology, stress, autonomic, nervous system disorders, blood-pressure reactivity, nerve activity, resistant hypertension, responses, muscle, ablation, arousal, task, htn, Pharmacology & Pharmacy, Cardiovascular System & Cardiology
Subject categories Cardiac and Cardiovascular Systems

Abstract

Background: The impact of renal denervation (RDN) on muscle sympathetic nerve activity (MSNA) at rest remains controversial. Mental stress (MS) induces transient changes in sympathetic nerve activity, heart rate (HR) and blood pressure (BP). It is not known whether RDN modifies these changes. Purpose: The main objective was to assess the effect of RDN on MSNA and BP alterations during MS. Methods: In 14 patients (11 included in analysis) with resistant hypertension multi-unit MSNA, BP (Finometer (R)) and HR were assessed at rest and during forced arithmetics at baseline and 6 months after RDN. Results: Systolic office BP decreased significantly 6 months after RDN (185 +/- 29 vs.175 +/- 33 mmHG; p = 0.04). No significant changes in MSNA at rest (68 +/- 5 vs 73 +/- 5 bursts/100hb; p = 0.43) were noted and no significant stress-induced change in group averaged sympathetic activity was found pre- (101 +/- 24%; p = 0.9) or post-intervention (108 +/- 26%; p = 0.37). Stress was associated with significant increases in mean arterial BP (p < 0.01) and HR (p < 0.01) at baseline, reactions which remained unaltered after intervention. We did not note any correlation between sympathetic nerve activity and BP changes after RDN. Conclusion: Thus, in our group of resistant hypertensives we find no support for the hypothesis that the BP-lowering effect of RDN depends on altered neurovascular responses to stress.

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