title: Substantial reduction in single sympathetic nerve firing after renal denervation in patients with resistant hypertension.
abstract: Renal denervation (RDN) has been shown to reduce blood pressure (BP) and muscle sympathetic nerve activity (MSNA) in patients with resistant hypertension. The mechanisms underlying sympathetic neural inhibition are unknown. We examined whether RDN differentially influences the sympathetic discharge pattern of vasoconstrictor neurons in patients with resistant hypertension. Standardized office BP, single-unit MSNA, and multi-unit MSNA were obtained at baseline and at 3-month follow-up in 35 patients with resistant hypertension. Twenty-five patients underwent RDN, and 10 patients underwent repeated measurements without RDN (non-RDN). Baseline BP averaged 164/93 mm Hg (RDN) and 164/87 mm Hg (non-RDN) despite use of an average of 4.8 ± 0.4 and 4.4 ± 0.5 antihypertensive drugs, respectively. Mean office BP decreased significantly by -13/-6 mm Hg for systolic BP (P<0.001) and diastolic BP (P<0.05) with RDN but not in non-RDN at 3-month follow-up. RDN moderately decreased multi-unit MSNA (79 ± 3 versus 73 ± 4 bursts/100 heartbeats; P<0.05), whereas all properties of single-unit MSNA including firing rates of individual vasoconstrictor fibers (43 ± 5 versus 27 ± 3 spikes/100 heartbeats; P<0.01), firing probability (30 ± 2 versus 22 ± 2% per heartbeat; P<0.02), and multiple firing incidence of single units within a cardiac cycle (8 ± 1 versus 4 ± 1% per heartbeat; P<0.05) were substantially reduced at follow-up. BP, single-unit MSNA, and multi-unit MSNA remained unaltered in the non-RDN cohort at follow-up. RDN results in the substantial and rapid reduction in firing properties of single sympathetic vasoconstrictor fibers, this being more pronounced than multi-unit MSNA inhibition. Whether the earlier changes in single-unit firing patterns may predict long-term BP response to RDN warrants further exploration.
authors.affiliation: Neurovascular Hypertension and Kidney Disease Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria 8008, Australia.
authors.forename: Dagmara
authors.initials: D
authors.lastname: Hering
authors.forename: Elisabeth A
authors.initials: EA
authors.lastname: Lambert
authors.forename: Petra
authors.initials: P
authors.lastname: Marusic
authors.forename: Antony S
authors.initials: AS
authors.lastname: Walton
authors.forename: Henry
authors.initials: H
authors.lastname: Krum
authors.forename: Gavin W
authors.initials: GW
authors.lastname: Lambert
authors.forename: Murray D
authors.initials: MD
authors.lastname: Esler
authors.forename: Markus P
authors.initials: MP
authors.lastname: Schlaich
mesh_terms: D001794:Blood Pressure / Q000502:physiology; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology / Q000601:surgery*; D007668:Kidney / Q000294:innervation* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009474:Neurons / Q000502:physiology*; D013562:Sympathectomy; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D016896:Treatment Outcome