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Postprandial hypotension (PPH) is a major clinical problem in patients with autonomic failure such as that observed in multiple system atrophy (MSA). The pathophysiology of PPH remains unclear, although autonomic dysfunction and gastrointestinal vasoactive peptides have been suspected to participate in its pathogenesis. We measured blood pressure and plasma levels of glucose, insulin, noradrenaline, neurotensin, glucagon-like peptide (GLP)-1 and GLP-2 before and after meal ingestion in 24 patients with MSA to reveal the roles of the autonomic nervous system and gastrointestinal vasoactive peptides in PPH. We performed a second meal-ingestion test by administering acarbose to evaluate the effects of acarbose (an α-glucosidase inhibitor) on PPH and vasoactive peptides in 14 patients with MSA and PPH. We also evaluated blood pressure responses to the head-up tilt test and heart rate variability in all the patients. Severities of PPH and orthostatic hypotension were significantly correlated. Patients with PPH had significantly worse orthostatic hypotension and lower heart rate variability than those without PPH. Postprandial GLP-1 secretion was higher in patients with PPH than in those without PPH. No significant differences were observed in the postprandial increases in plasma levels of glucose, insulin, noradrenaline, neurotensin or GLP-2. Acarbose significantly attenuated postprandial hypotension and tended to decrease GLP-2 secretion. Our results indicate that autonomic failure is involved in the pathogenesis of PPH and confirm that acarbose has a preventive effect against PPH in patients with MSA. Decreased postprandial secretion of GLP-2, which increases intestinal blood pooling, may attenuate PPH in patients with MSA.

On head down tilt to the supine horizontal position (tilt reversal) after head up tilt (HUT), patients with orthostatic hypotension may show an increase in blood pressure (BP) relative to baseline readings. We assessed this BP overshoot in 8 patients with pure autonomic failure (PAF, 64+/-13 years) and 8 patients with multiple system atrophy (MSA, 66+/-10 years). BP was intermittently measured during pre-tilt supine, HUT (60 degrees , 10 min), and post-tilt supine periods. In addition, beat-to-beat BP was measured continuously using the Portapres model 2 device to calculate stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR). There was systolic BP overshoot of > or = 15 mmHg after tilt reversal in 5 out of 8 PAF, but in only one of 8 MSA. A mean increase of systolic BP in PAF was significantly higher than that in MSA (p<0.01). TPR increased over baseline level after tilt reversal, although there was no significant difference. SV and CO levels during the post-tilt supine period were similar to baseline levels. In conclusion, BP overshoot was prominent in the PAF group but not in the MSA group. The phenomenon of BP overshoot while supine, especially in PAF, may have implications for long term cardiac and vascular damage in such patients.