Non-alpha-adrenergic effects on systemic vascular conductance during lower-body negative pressure, static exercise and muscle metaboreflex activation

Aim This study tested the hypothesis that non‐α‐adrenergic mechanisms contribute to systemic vascular conductance (SVC) in a reflex‐specific manner during the sympathoexcitatory manoeuvres. Methods Twelve healthy subjects underwent lower‐body negative pressure (LBNP, −40 mmHg) as well as static hand...

Full description

Saved in:
Bibliographic Details
Published in:Acta Physiologica Vol. 206; no. 1; pp. 51 - 61
Main Authors: Kiviniemi, A. M., Frances, M. F., Rachinsky, M., Craen, R., Petrella, R. J., Huikuri, H. V., Tulppo, M. P., Shoemaker, J. K.
Format: Journal Article
Language:English
Published: Oxford Blackwell Publishing Ltd 01.09.2012
Wiley-Blackwell
Wiley Subscription Services, Inc
Subjects:
Adrenergic alpha-Antagonists - pharmacology
Adrenergic Neurons - physiology
Adult
arterial pressure regulation
Biological and medical sciences
Exercise - physiology
Female
Fundamental and applied biological sciences. Psychology
Heart Rate - physiology
Humans
Lower Body Negative Pressure
Male
Muscle, Skeletal - drug effects
Muscle, Skeletal - physiology
phentolamine
Phentolamine - pharmacology
sympathetic activity
Sympathetic Nervous System - physiology
Vasoconstriction - physiology
Vertebrates: anatomy and physiology, studies on body, several organs or systems
Physical exercise
arterial pressure regulation
α1-Adrenergic receptor
sympathetic activity
Activation
Negative pressure
Striated muscle
Sympathetic nervous system
Vertebrata
Alpha blocking agent
Mammalia
Metaboreflex
Autonomic nervous system
Arterial pressure
Antagonist
Hemodynamics
Phentolamine
ISSN:1748-1708, 1748-1716, 1748-1716
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Aim This study tested the hypothesis that non‐α‐adrenergic mechanisms contribute to systemic vascular conductance (SVC) in a reflex‐specific manner during the sympathoexcitatory manoeuvres. Methods Twelve healthy subjects underwent lower‐body negative pressure (LBNP, −40 mmHg) as well as static handgrip exercise (HG, 20% of maximal force) followed by post‐exercise forearm circulatory occlusion (PECO, 5 min each) with and without α‐adrenergic blockade induced by phentolamine (PHE). Aortic blood flow, finger blood pressure and superficial femoral artery blood flow were measured to calculate cardiac output, SVC and leg vascular conductance (LVC) during the last minute of each intervention. Results Mean arterial pressure (MAP) decreased more during LBNP with PHE compared with saline (−7 ± 7 vs. −2 ± 5%, P = 0.016). PHE did not alter the MAP response to HG (+20 ± 12 and +24 ± 16%, respectively, for PHE and saline) but decreased the change in MAP during PECO (+12 ± 7 vs. +21 ± 14%, P = 0.005). The decrease in SVC and LVC with LBNP did not differ between saline and PHE trials (−13 ± 10 vs. −17 ± 10%, respectively, for SVC, P = 0.379). In contrast, the SVC response to HG increased from −9 ± 12 with saline to + 5 ± 15% with PHE (P = 0.002) and from −16 ± 15 with saline to +1 ± 16% with PHE during PECO (P = 0.003). LVC responses to HG or PECO were not different from saline with PHE. Conclusions Non‐α‐adrenergic vasoconstriction was present during LBNP. The systemic vasoconstriction during static exercise and isolated muscle metaboreflex activation, in the absence of leg vasoconstriction, was explained by an α‐adrenergic mechanism. Therefore, non‐α‐adrenergic vasoconstriction is more emphasized during baroreflex, but not metaboreflex‐mediated sympathetic activation.
Bibliography:ark:/67375/WNG-8MLVZLLW-M
Finnish Technology Development Centre
istex:61A1A21661A4B4BB1A349893DC86518CAB7B524A
Paavo Nurmi Foundation
Finnish Foundation of Cardiovascular Research
Canadian Institutes of Health Research
Research Council for Health of the Academy of Finland
ArticleID:APHA2447
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
ISSN:1748-1708
1748-1716
1748-1716
DOI:10.1111/j.1748-1716.2012.02447.x