Levodopa is a precursor of dopamine and therefore of norepinephrine (NE), the sympathetic neurotransmitter. In the treatment of PD, levodopa is usually combined with an inhibitor of L-aromatic-acid-decarboxylase that does not penetrate the blood-brain barrier. The combined treatment augments delivery of levodopa to the brain and mitigates nausea and vomiting thought to result from occupation of dopamine receptors outside the blood-brain barrier. Such treatment attenuates but does not prevent catechol-amine synthesis from levodopa outside the brain. Neurocirculatory abnormalities underlying OH might therefore might reflect levo-dopa treatment.
To test this hypothesis, we carried out tests of reflexive cardiovagal gain (decrease in interbeat interval per unit decrease in systolic pressure during the Valsalva maneuver; orthostatic increase in heart rate per unit decrease in pressure); and reflexive sympatho-neural function (decrease in pressure during the Valsalva maneuver; orthostatic increment in plasma NE) in PD patients without or with OH who were off or on levodopa at the time of testing. Severity of orthostatic hypotension did not differ between the levodopa-untreated and levodopa-treated groups with PD + OH. The two groups had similarly low reflexive cardiovagal gain during the Valsalva maneuver and during orthostasis and had similarly attenuated reflexive plasma NE responses during both manipulations. Low values for reflexive cardiovagal gain and sympatho-neural responses were strongly related to
orthostatic hypotension. PD + OH therefore features reflexive cardiovagal and sympatho-neural failure, independently of levodopa treatment (Goldstein et al., 2005).
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