Pharmacological evidence of alpha₁- and alpha₂-adrenergic supersensitivity in orthostatic hypotension due to spinal cord injury: a case report

Summary

Sympathetic efferent pathways and alpha-adrenergic receptivity were investigated in one patient with spinal cord transection (D1 level) and orthostatic hypotension. The lack of increase in catecholamine plasma levels during orthostasis and the paradoxical pressor effect of clonidine (2 μg/kg orally) suggested complete interruption of efferent sympathetic pathways.

The pressor response to exogenous noradrenaline was significantly higher in the patient than in 6 normal controls (0.09 vs 0.72 μg·kg⁻¹), indicating supersensitivity of vascular α-adrenoceptors. The platelet α₂-adrenergic receptor number, measured with [³H]yohimbine, was 507 in the patient vs 178 fmol·mg⁻¹ protein in controls. The increase in systolic blood pressure induced by 10 mg midodrine, a specific α₁-agonist, was significantly higher in the patient (δ=56 mm Hg) than in controls (δ=15 mm Hg).

The results indicate that in the patient there was α-adrenergic supersensitivity both of α₁- and α₂-adrenoceptors. This led to successfully oral treatment of the orthostatic hypotension with clonidine 150 μg bd and midodrine 10 mg bd.