دورية أكاديمية
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Central α 2 -adrenergic mechanisms regulate human sympathetic neuronal discharge strategies.

التفاصيل البيبلوغرافية
العنوان: Central α 2 -adrenergic mechanisms regulate human sympathetic neuronal discharge strategies.
المؤلفون: Klassen SA; Sympathetic Neurocirculatory Regulation Laboratory, Department of Kinesiology, Brock University, St Catharines, ON, Canada., Limberg JK; Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO, USA., Harvey RE; Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, MN, USA., Wiggins CC; Department of Kinesiology, Michigan State University, East Lansing, MI, USA., Iannarelli NJ; Sympathetic Neurocirculatory Regulation Laboratory, Department of Kinesiology, Brock University, St Catharines, ON, Canada., Senefeld JW; Department of Health and Kinesiology, Beckman Institute for Advanced Science and Technology, University of Illinois Urbana-Champaign, University of Illinois at Urbana-Champaign, Champaign, IL, USA., Nicholson WT; Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, MN, USA., Curry TB; Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, MN, USA., Joyner MJ; Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, MN, USA., Shoemaker JK; School of Kinesiology, Department of Physiology and Pharmacology, University of Western Ontario, London, ON, Canada., Baker SE; Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, MN, USA.
المصدر: The Journal of physiology [J Physiol] 2024 Aug; Vol. 602 (16), pp. 4053-4071. Date of Electronic Publication: 2024 Jul 26.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Cambridge Univ. Press Country of Publication: England NLM ID: 0266262 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1469-7793 (Electronic) Linking ISSN: 00223751 NLM ISO Abbreviation: J Physiol Subsets: MEDLINE
أسماء مطبوعة: Publication: Oxford : Blackwell : Cambridge Univ. Press
Original Publication: London, Cambridge Univ. Press.
مواضيع طبية MeSH: Dexmedetomidine*/pharmacology , Adrenergic alpha-2 Receptor Agonists*/pharmacology , Sympathetic Nervous System*/physiology , Sympathetic Nervous System*/drug effects , Action Potentials*/drug effects , Action Potentials*/physiology, Humans ; Female ; Adult ; Male ; Young Adult ; Heart Rate/drug effects ; Heart Rate/physiology ; Blood Pressure/physiology ; Blood Pressure/drug effects ; Muscle, Skeletal/physiology ; Muscle, Skeletal/innervation ; Muscle, Skeletal/drug effects ; Receptors, Adrenergic, alpha-2/physiology ; Receptors, Adrenergic, alpha-2/metabolism
مستخلص: The present study investigated the impact of central α 2 -adrenergic mechanisms on sympathetic action potential (AP) discharge, recruitment and latency strategies. We used the microneurographic technique to record muscle sympathetic nerve activity and a continuous wavelet transform to investigate postganglionic sympathetic AP firing during a baseline condition and an infusion of a α 2 -adrenergic receptor agonist, dexmedetomidine (10 min loading infusion of 0.225 µg kg -1 ; maintenance infusion of 0.1-0.5 µg kg h -1 ) in eight healthy individuals (28 ± 7 years, five females). Dexmedetomidine reduced mean pressure (92 ± 7 to 80 ± 8 mmHg, P < 0.001) but did not alter heart rate (61 ± 13 to 60 ± 14 bpm; P = 0.748). Dexmedetomidine reduced sympathetic AP discharge (126 ± 73 to 27 ± 24 AP 100 beats -1 , P = 0.003) most strongly for medium-sized APs (normalized cluster 2: 21 ± 10 to 5 ± 5 AP 100 beats -1 ; P < 0.001). Dexmedetomidine progressively de-recruited sympathetic APs beginning with the largest AP clusters (12 ± 3 to 7 ± 2 clusters, P = 0.002). Despite de-recruiting large AP clusters with shorter latencies, dexmedetomidine reduced AP latency across remaining clusters (1.18 ± 0.12 to 1.13 ± 0.13 s, P = 0.002). A subset of six participants performed a Valsalva manoeuvre (20 s, 40 mmHg) during baseline and the dexmedetomidine infusion. Compared to baseline, AP discharge (Δ 361 ± 292 to Δ 113 ± 155 AP 100 beats -1 , P = 0.011) and AP cluster recruitment elicited by the Valsalva manoeuvre were lower during dexmedetomidine (Δ 2 ± 1 to Δ 0 ± 2 AP clusters, P = 0.041). The reduction in sympathetic AP latency elicited by the Valsalva manoeuvre was not affected by dexmedetomidine (Δ -0.09 ± 0.07 to Δ -0.07 ± 0.14 s, P = 0.606). Dexmedetomidine reduced baroreflex gain, most strongly for medium-sized APs (normalized cluster 2: -6.0 ± 5 to -1.6 ± 2 % mmHg -1 ; P = 0.008). These data suggest that α 2 -adrenergic mechanisms within the central nervous system modulate sympathetic postganglionic neuronal discharge, recruitment and latency strategies in humans. KEY POINTS: Sympathetic postganglionic neuronal subpopulations innervating the human circulation exhibit complex patterns of discharge, recruitment and latency. However, the central neural mechanisms governing sympathetic postganglionic discharge remain unclear. This microneurographic study investigated the impact of a dexmedetomidine infusion (α 2 -adrenergic receptor agonist) on muscle sympathetic postganglionic action potential (AP) discharge, recruitment and latency patterns. Dexmedetomidine infusion inhibited the recruitment of large and fast conducting sympathetic APs and attenuated the discharge of medium sized sympathetic APs that fired during resting conditions and the Valsalva manoeuvre. Dexmedetomidine infusion elicited shorter sympathetic AP latencies during resting conditions but did not affect the reductions in latency that occurred during the Valsalva manoeuvre. These data suggest that α 2 -adrenergic mechanisms within the central nervous system modulate sympathetic postganglionic neuronal discharge, recruitment and latency strategies in humans.
(© 2024 The Author(s). The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)
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معلومات مُعتمدة: F32 HL154320 United States HL NHLBI NIH HHS; AHA15SDG2508009 American Heart Association (AHA); 00320 Canadian Government | Natural Sciences and Engineering Research Council of Canada (NSERC); R35 HL139854 United States HL NHLBI NIH HHS; T32 DK007352 United States DK NIDDK NIH HHS; T32-DK-007352 HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); F32-HL-154320 HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI); 217916 Canadian Government | Natural Sciences and Engineering Research Council of Canada (NSERC); 05293 Canadian Government | Natural Sciences and Engineering Research Council of Canada (NSERC); K01-HL-148144 HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI); K01 HL148144 United States HL NHLBI NIH HHS; R-35-HL-139854 HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)
فهرسة مساهمة: Keywords: action potential; dexmedetomidine; human; microneurography; muscle sympathetic nerve activity; valsalva manoeuvre; α2‐adrenergic receptors
المشرفين على المادة: 67VB76HONO (Dexmedetomidine)
0 (Adrenergic alpha-2 Receptor Agonists)
0 (Receptors, Adrenergic, alpha-2)
تواريخ الأحداث: Date Created: 20240726 Date Completed: 20240815 Latest Revision: 20240821
رمز التحديث: 20240822
مُعرف محوري في PubMed: PMC11326960
DOI: 10.1113/JP286450
PMID: 39058701
قاعدة البيانات: MEDLINE
الوصف
تدمد:1469-7793
DOI:10.1113/JP286450