title: Role of intestinal peptides and the autonomic nervous system in postprandial hypotension in patients with multiple system atrophy.
abstract: 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.
authors.affiliation: Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Fukushima
authors.forename: Masato
authors.initials: M
authors.lastname: Asahina
authors.forename: Yoshikatsu
authors.initials: Y
authors.lastname: Fujinuma
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Yamanaka
authors.forename: Akira
authors.initials: A
authors.lastname: Katagiri
authors.forename: Masahiro
authors.initials: M
authors.lastname: Mori
authors.forename: Satoshi
authors.initials: S
authors.lastname: Kuwabara
mesh_terms: D020909:Acarbose / Q000494:pharmacology; D000368:Aged; D000704:Analysis of Variance; D001342:Autonomic Nervous System Diseases / Q000097:blood / Q000150:complications / Q000209:etiology; D001786:Blood Glucose / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D052216:Glucagon-Like Peptide 1 / Q000097:blood*; D053767:Glucagon-Like Peptide 2 / Q000097:blood*; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007022:Hypotension / Q000209:etiology* / Q000534:rehabilitation; D007328:Insulin / Q000097:blood; D008297:Male; D008875:Middle Aged; D019578:Multiple System Atrophy / Q000097:blood / Q000150:complications* / Q000534:rehabilitation; D009496:Neurotensin / Q000097:blood; D019518:Postprandial Period / Q000187:drug effects
chemical_list: D001786:Blood Glucose; D053767:Glucagon-Like Peptide 2; D007004:Hypoglycemic Agents; D007328:Insulin; D009496:Neurotensin; D052216:Glucagon-Like Peptide 1; D020909:Acarbose