Beta adrenergic influence on esophageal and colonic motility in man.
Gastrointestinal (GI) motility is centrally controlled through the sympathetic and parasympathetic nerves, sympathetic effects being partly mediated by beta adrenoceptors. Although beta adrenoceptor agonists and antagonists are widely used for different disorders, little is known about the influence of these agents on GI motility. The present study was initiated to investigate whether there is a physiological, beta adrenergic influence on human GI motility and to describe the effects of selective beta adrenoceptor stimulation on motility in the proximal and distal parts of the GI tract. Esophageal peristalsis was measured in healthy subjects using electronic catheters. Distal colonic motility was measured with an open-tipped, water-perfused catheter in the sigmoid colon and from an air-filled balloon in the rectum in healthy subjects and in patients with the irritable bowel syndrome (IBS). In one study, colonic motility was stimulated with continuous infusion of the octapeptide of cholecystokinin (CCK-OP). Esophagus: Peristaltic amplitude was increased in the distal smooth muscle part of the esophageal body after infusion of both the nonselective beta blocker propranolol and the beta-1 selective blocker metoprolol. After infusion of the beta-1 agonist prenalterol and the beta-2 selective agonist terbutaline, a profound decrease in esophageal peristaltic amplitude was seen. Pretreatment with metoprolol selectively blocked the response to a moderate dose of prenalterol but did not block the response to terbutaline. The latter response was blocked by propranolol. Peristaltic velocity in the proximal part of the esophagus was decreased by beta-1 stimulation and in the distal part by beta-2 stimulation. Distal colon: In healthy subjects the sigmoid motility index showed a dose-dependent increase after metoprolol and propranolol, respectively. The increase was more marked after propranolol infusion. Terbutaline decreased the sigmoid motility index both in healthy subjects and in patients with the IBS. Furthermore, the rectal motility index was decreased in the group of healthy subjects. The effects of prenalterol on rectal and sigmoid motility did not differ from those of placebo. The IBS patient group showed larger intraindividual variations in sigmoid motility from day to day and also lower rectal motility indices than the healthy subjects. Infusion of CCK-OP increased the sigmoid motility index compared to non-stimulated conditions. No effects on CCK-OP stimulated motility were seen after either terbutaline, prenalterol or placebo.(ABSTRACT TRUNCATED AT 400 WORDS)
Lyrenäs
E
E
D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000328:Adult; D003106:Colon / Q000187:drug effects*; D003109:Colonic Diseases, Functional / Q000503:physiopathology; D004947:Esophagus / Q000187:drug effects*; D005260:Female; D005769:Gastrointestinal Motility / Q000187:drug effects*; D006801:Humans; D008297:Male; D008365:Manometry; D008790:Metoprolol / Q000494:pharmacology; D008875:Middle Aged; D010276:Parasympatholytics / Q000494:pharmacology; D011217:Practolol / Q000031:analogs & derivatives / Q000494:pharmacology; D011294:Prenalterol; D011433:Propranolol / Q000494:pharmacology; D012844:Sincalide / Q000494:pharmacology; D013726:Terbutaline / Q000494:pharmacology
D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D010276:Parasympatholytics; D011433:Propranolol; D008790:Metoprolol; D012844:Sincalide; D011294:Prenalterol; D013726:Terbutaline; D011217:Practolol