Postprandial hypotension in de novo Parkinson's disease: A comparison with orthostatic hypotension

Abstract

BackgroundPostprandial hypotension (PPH) is often associated with Parkinson's disease (PD). However, its mechanism remains to be fully defined. We investigated the mechanism of PPH and compared it with that of orthostatic hypotension (OH). MethodsThe subjects were 37 patients with de novo PD and 10 healthy age-matched controls. We studied changes in blood pressure (BP), plasma norepinephrine concentrations (NE), plasma insulin, plasma glucose concentrations during a 75-g oral glucose tolerance test (75-g OGTT). Changes in BP and NE were also examined with head-up tilt-table testing (HUT). ResultsThe maximum fall in systolic BP (SBP) on 75-g OGTT (⊿SBPPPH) significantly correlated with that on HUT (r = 0.359, p < 0.05). On 75-g OGTT, ⊿SBPPPH significantly correlated with SBP after 20 min of rest in the supine position (r = 0.394, p < 0.01) and the time in which SBP reached its lowest (r = 0.436, p < 0.01). ⊿SBPPPH did not correlate with NE, plasma insulin and glucose concentrations after glucose loading, but significantly negatively correlated with NE measured after 20 min resting in the supine position (r = −0.347, p < 0.05). Clinical characteristics, including the presence of constipation, did not differ significantly between patients with and those without PPH. ConclusionsIn PD, systemic sympathetic denervation, impaired baroreflex-cardiovagal gain, and insufficiency of compensatory sympathetic nervous activation including lack of baroreflex-sympathoneural gain for postprandial splanchnic vessel pooling seem to be associated with PPH. Systemic sympathetic denervation and baroreflex failure seem to contribute to both pronounced morbidity and the development of PPH and OH.