OBJECTIVE: Spinal cord-injured (SCI) individuals demonstrate an increased baseline leg vascular resistance (LVR). In addition, despite the lack of sympathetic control, an increase in LVR is observed during orthostatic challenges. On the basis of the vasoconstrictive characteristics of angiotensin II, we examined the hypothesis that angiotensin II contributes to the LVR at baseline and during head-up tilt (HUT) in SCI individuals. METHODS: Supine baseline leg and forearm blood flow were measured using venous occlusion plethysmography and leg blood flow during 30° HUT using duplex ultrasound. Measurements were performed before and 4 h after an angiotensin II antagonist (irbesartan, 150 mg) administered in eight SCI individuals and eight age-matched and sex-matched able-bodied controls. Vascular resistance was calculated as the arterial-venous pressure gradient divided by blood flow. RESULTS: Angiotensin II blockade significantly decreased baseline LVR in SCI individuals (P = 0.02) but not in controls, whereas no changes in forearm vascular resistance were found in both groups. Angiotensin II blockade did not alter the increase in LVR during HUT in SCI individuals nor in controls. CONCLUSION: Our results indicate that angiotensin II contributes to the increased baseline LVR in SCI individuals. As angiotensin II does not contribute to forearm vascular resistance, the contribution to LVR may relate to the extreme inactivity of the legs in SCI individuals. Angiotensin II does not contribute to the increase in LVR during HUT in SCI individuals nor in controls.
OBJECTIVE: Spinal cord-injured (SCI) individuals demonstrate an increased baseline leg vascular resistance (LVR). In addition, despite the lack of sympathetic control, an increase in LVR is observed during orthostatic challenges. On the basis of the vasoconstrictive characteristics of angiotensin II, we examined the hypothesis that angiotensin II contributes to the LVR at baseline and during head-up tilt (HUT) in SCI individuals. METHODS: Supine baseline leg and forearm blood flow were measured using venous occlusion plethysmography and leg blood flow during 30° HUT using duplex ultrasound. Measurements were performed before and 4 h after an angiotensin II antagonist (irbesartan, 150 mg) administered in eight SCI individuals and eight age-matched and sex-matched able-bodied controls. Vascular resistance was calculated as the arterial-venous pressure gradient divided by blood flow. RESULTS:Angiotensin II blockade significantly decreased baseline LVR in SCI individuals (P = 0.02) but not in controls, whereas no changes in forearm vascular resistance were found in both groups. Angiotensin II blockade did not alter the increase in LVR during HUT in SCI individuals nor in controls. CONCLUSION: Our results indicate that angiotensin II contributes to the increased baseline LVR in SCI individuals. As angiotensin II does not contribute to forearm vascular resistance, the contribution to LVR may relate to the extreme inactivity of the legs in SCI individuals. Angiotensin II does not contribute to the increase in LVR during HUT in SCI individuals nor in controls.
Authors: A A Phillips; N Matin; B Frias; M M Z Zheng; M Jia; C West; A M Dorrance; I Laher; A V Krassioukov Journal: J Physiol Date: 2016-01-18 Impact factor: 5.182
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Authors: Gurpreet K Birk; Ellen A Dawson; N Timothy Cable; Daniel J Green; Dick H J Thijssen Journal: Eur J Appl Physiol Date: 2012-09-29 Impact factor: 3.078
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