Spinal cord injury enhances arterial expression and reactivity of α1-adrenergic receptors-mechanistic investigation into autonomic dysreflexia

BACKGROUND CONTEXT: Autonomic dysreflexia (AD) usually presents with a significant increase in blood pressure, and uncontrollable autonomic response to stimuli below the level of spinal cord injury (SCI). PURPOSE: This study analyzed the vasomotor function and molecular changes in the peripheral arteries below the lesion of SCI to characterize the mechanism of autonomic dysreflexia. STUDY DESIGN: This was a randomized experimental study in rats. METHODS: Contusive SCI was induced using a force-calibrated weight-drop device at the T10 level in anesthetized rats. Two weeks after severe SCI, blood flow in the femoral arteries was measured, and the vasomotor function and expression of alpha 1-adrenergic receptors were analyzed. RESULTS: Blood flow in the femoral artery was significantly reduced in rats with SCI (8.0 +/- 2 vs. 17.5 +/- 4 mL/min, SCI vs. control, respectively; p=.016). The contraction responses of femoral artery segments to cumulative addition of alpha 1-adrenergic agonist phenylephrine were significantly enhanced in rats with SCI. Expression of alpha 1-adrenergic receptor was upregulated in the medial layer of femoral artery vascular homogenates of these rats. CONCLUSION: Our study provides evidence demonstrating that prolonged denervation below the lesion level following SCI results in a compensatory increased expression of alpha 1-adrenergic receptors in the arterial smooth muscle layer, thereby enhancing the responsiveness to alpha 1-adrenergic agonist and potentiating the development of AD. (C) 2015 Elsevier Inc. All rights reserved.