title: Microneurographic evidence in healthy middle-aged humans for a sympathoexcitatory reflex activated by atrial pressure.
abstract: Atrial mechanoreceptors, stimulated by increased pressure or volume, elicit in healthy humans a net sympathoinhibitory response. The co-existence of an atrial reflex eliciting muscle sympathoexcitation has been postulated but undetected by conventional multi-unit muscle sympathetic nerve activity (MSNA). We hypothesized that in response to a selective increase in atrial pressure, single-unit MSNA would reveal a subpopulation of efferent sympathetic neurons with firing patterns opposite to the integrated multi-unit MSNA envelope. Multi- and single-unit MSNA recordings were acquired in eight healthy middle-aged subjects (age, 57 ± 8 years; body mass index, 25 ± 2 kg/m(2)) submitted to selective decreases or increases in atrial pressure by nonhypotensive lower body negative pressure (LBNP; -10 mmHg) or nonhypertensive lower body positive pressure (LBPP; +10 mmHg), respectively. Single-unit MSNA firing responses were classified as anticipated if spike frequency and incidence increased with LBNP or decreased with LBPP and paradoxical if they decreased with LBNP or increased with LBPP. LBNP decreased (3.2 ± 2.8 to 1.4 ± 3.1 mmHg, P < 0.01) and LBPP increased (3.3 ± 2.7 to 4.9 ± 2.8 mmHg, P < 0.01) estimated central venous pressure without affecting stroke volume, systemic pressure, or resistance. Multi-unit MSNA increased with LBNP (31 ± 17 to 38 ± 19 bursts/min, P < 0.01) and diminished with LBPP (33 ± 15 to 28 ± 15 bursts/min, P < 0.01). Of 21 single-units identified, 76% exhibited firing responses to both LBNP and LBPP concordant with multi-unit MSNA, whereas 24% demonstrated discordant or paradoxical responses. The detection of two subpopulations of single-units within the multi-unit MSNA recording, exhibiting opposite firing characteristics, establishes the first evidence in humans for the existence of an excitatory cardiac-muscle sympathetic reflex activated by increasing atrial pressure.
authors.affiliation: University Health Network and Mount Sinai Hospital Division of Cardiology, University of Toronto, Toronto, Ontario, Canada.
authors.forename: Philip J
authors.initials: PJ
authors.lastname: Millar
authors.forename: Hisayoshi
authors.initials: H
authors.lastname: Murai
authors.forename: Beverley L
authors.initials: BL
authors.lastname: Morris
authors.forename: John S
authors.initials: JS
authors.lastname: Floras
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D016275:Atrial Function / Q000502:physiology*; D062185:Atrial Pressure / Q000502:physiology*; D017704:Baroreflex / Q000502:physiology*; D004568:Electrodiagnosis / Q000379:methods; D005260:Female; D006325:Heart Atria / Q000294:innervation; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008297:Male; D040542:Mechanotransduction, Cellular / Q000502:physiology*; D008875:Middle Aged; D013564:Sympathetic Nervous System / Q000502:physiology*
keywords: atrial pressure; cardiopulmonary reflex; muscle sympathetic nerve activity