| Sympathetic nonadrenergic transmission contributes to autonomic dysreflexia in spinal cord-injured individuals. | |
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MedLine Citation:
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PMID: 20100992 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't Date: 2010-01-25 |
Journal Detail:
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Title: Hypertension Volume: 55 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2010 Mar |
Date Detail:
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Created Date: 2010-02-19 Completed Date: 2010-03-18 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 636-43 Citation Subset: IM |
Affiliation:
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Department of Physiology, Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adrenergic alpha-Antagonists
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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:
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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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