Document Detail


Sympathetic nonadrenergic transmission contributes to autonomic dysreflexia in spinal cord-injured individuals.
MedLine Citation:
PMID:  20100992     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Autonomic dysreflexia is a hypertensive episode in spinal cord-injured individuals induced by exaggerated sympathetic activity and thought to be alpha-adrenergic mediated. alpha-Adrenoceptor antagonists have been a rational first choice; nevertheless, calcium channel blockers are primarily used in autonomic dysreflexia management. However, alpha-adrenoceptor blockade may leave a residual vasoconstrictor response to sympathetic nonadrenergic transmission unaffected. The aim was to assess the alpha-adrenergic contribution and, in addition, the role of supraspinal control to leg vasoconstriction during exaggerated sympathetic activity provoked by autonomic dysreflexia in spinal cord-injured individuals and by a cold pressure test in control individuals. Upper leg blood flow was measured using venous occlusion plethysmography during supine rest and during exaggerated sympathetic activity in 6 spinal cord-injured individuals and 7 able-bodied control individuals, without and with phentolamine (alpha-adrenoceptor antagonist) and nicardipine (calcium channel blocker) infusion into the right femoral artery. Leg vascular resistance was calculated. In spinal cord-injured individuals, phentolamine significantly reduced the leg vascular resistance increase during autonomic dysreflexia (8+/-5 versus 24+/-13 arbitrary units; P=0.04) in contrast to nicardipine (15+/-10 versus 24+/-13 arbitrary units; P=0.12). In controls, phentolamine completely abolished the leg vascular resistance increase during a cold pressure test (1+/-2 versus 18+/-14 arbitrary units; P=0.02). The norepinephrine increase during phentolamine infusion was larger (P=0.04) in control than in spinal cord-injured individuals. These results indicate that the leg vascular resistance increase during autonomic dysreflexia in spinal cord-injured individuals is not entirely alpha-adrenergic mediated and is partly explained by nonadrenergic transmission, which may, in healthy subjects, be suppressed by supraspinal control.
Authors:
Jan T Groothuis; Gerard A Rongen; Jaap Deinum; Peter Pickkers; A H Jan Danser; Alexander C H Geurts; Paul Smits; Maria T E Hopman
Publication Detail:
Type:  Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-01-25
Journal Detail:
Title:  Hypertension     Volume:  55     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-02-19     Completed Date:  2010-03-18     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  636-43     Citation Subset:  IM    
Affiliation:
Department of Physiology, Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic alpha-Antagonists / administration & dosage*
Adult
Aged
Angiotensin II / blood
Autonomic Dysreflexia* / drug therapy,  etiology,  physiopathology
Autonomic Nervous System Diseases* / complications,  drug therapy,  physiopathology
Blood Pressure / drug effects,  physiology
Calcium Channel Blockers / administration & dosage
Humans
Leg / blood supply
Male
Middle Aged
Nicardipine / administration & dosage
Norepinephrine / blood
Phentolamine / administration & dosage*
Plethysmography
Receptors, Adrenergic, alpha / physiology
Regional Blood Flow / drug effects,  physiology
Renin / blood
Spinal Cord Injuries / complications*,  physiopathology*
Vascular Resistance / drug effects,  physiology
Young Adult
Chemical
Reg. No./Substance:
0/Adrenergic alpha-Antagonists; 0/Calcium Channel Blockers; 0/Receptors, Adrenergic, alpha; 11128-99-7/Angiotensin II; 50-60-2/Phentolamine; 51-41-2/Norepinephrine; 55985-32-5/Nicardipine; EC 3.4.23.15/Renin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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