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- Horacio Kaufmann.
- Dysautonomia Research Laboratory, New York University School of Medicine, 530 First Avenue, New York, NY 10016, USA. horacio.kaufmann@med.nyu.edu
- Clin. Auton. Res. 2008 Mar 1; 18 Suppl 1: 19-24.
AbstractNeurogenic orthostatic hypotension results from failure to release norepinephrine, the neurotransmitter of sympathetic postganglionic neurons, appropriately upon standing. In double blind, cross over, placebo controlled trials, administration of droxidopa, a synthetic amino acid that is decarboxylated to norepinephrine by the enzyme L: -aromatic amino acid decarboxylase increases standing blood pressure, ameliorates symptoms of orthostatic hypotension and improves standing ability in patients with neurogenic orthostatic hypotension due to degenerative autonomic disorders. The pressor effect results from conversion of droxidopa to norepinephrine outside the central nervous system both in neural and non-neural tissue. This mechanism of action makes droxidopa effective in patients with central and peripheral autonomic disorders.
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