Sympathetic Nonadrenergic Transmission Contributes to Autonomic Dysreflexia in Spinal Cord-Injured Individuals

JT Groothuis; GA Rongen; J (Jacob) Deinum; P Pickkers; Jan Danser; ACH Geurts; P Smits; MTE Hopman

doi:10.1161/HYPERTENSIONAHA.109.147330

Sympathetic Nonadrenergic Transmission Contributes to Autonomic Dysreflexia in Spinal Cord-Injured Individuals

JT Groothuis, GA Rongen, J (Jacob) Deinum, P Pickkers, Jan Danser, ACH Geurts, P Smits, MTE Hopman

Internal Medicine

Research output: Contribution to journal › Article › Academic › peer-review

15 Citations (Scopus)

Abstract

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. (Hypertension. 2010; 55: 636-643.)

Original language	Undefined/Unknown
Pages (from-to)	636-643
Number of pages	8
Journal	Hypertension
Volume	55
Issue number	3
DOIs	https://doi.org/10.1161/HYPERTENSIONAHA.109.147330
Publication status	Published - 2010

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10.1161/HYPERTENSIONAHA.109.147330

http://hdl.handle.net/1765/19916

Cite this

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title = "Sympathetic Nonadrenergic Transmission Contributes to Autonomic Dysreflexia in Spinal Cord-Injured Individuals",

abstract = "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. (Hypertension. 2010; 55: 636-643.)",

author = "JT Groothuis and GA Rongen and Deinum, {J (Jacob)} and P Pickkers and Jan Danser and ACH Geurts and P Smits and MTE Hopman",

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doi = "10.1161/HYPERTENSIONAHA.109.147330",

language = "Undefined/Unknown",

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T1 - Sympathetic Nonadrenergic Transmission Contributes to Autonomic Dysreflexia in Spinal Cord-Injured Individuals

AU - Groothuis, JT

AU - Rongen, GA

AU - Deinum, J (Jacob)

AU - Pickkers, P

AU - Danser, Jan

AU - Geurts, ACH

AU - Smits, P

AU - Hopman, MTE

PY - 2010

Y1 - 2010

N2 - 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. (Hypertension. 2010; 55: 636-643.)

AB - 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. (Hypertension. 2010; 55: 636-643.)

U2 - 10.1161/HYPERTENSIONAHA.109.147330

DO - 10.1161/HYPERTENSIONAHA.109.147330

M3 - Article

C2 - 20100992

SN - 0194-911X

VL - 55

SP - 636

EP - 643

JO - Hypertension

JF - Hypertension

IS - 3

ER -