Failure of beta-adrenergic stimulation to affect cholecystokinin-stimulated sigmoid motility in man
- PMID: 2869574
- DOI: 10.3109/00365528509089271
Failure of beta-adrenergic stimulation to affect cholecystokinin-stimulated sigmoid motility in man
Abstract
Sigmoid motility, stimulated by the octapeptide of cholecystokinin (OP-CCK) and the effects of beta-adrenoceptor agonists, was studied in 12 healthy subjects in a randomized, double-blind fashion. Sigmoid pressure was recorded 18-20 cm from the anus, and contractile activity quantified as the area under pressure waves for three 25-min periods. OP-CCK (sincalide), 80 ng X kg-1 X h-1, was continuously infused throughout each session, resulting in a high sigmoid motility index. Preceded by a control period, terbutaline (beta-2 agonist), prenalterol (beta-1 agonist), or placebo was injected on 3 separate days. After 1 mg + 4 mg prenalterol or 0.25 mg + 0.25 mg terbutaline intravenously no significant changes in motility pattern were seen compared with the control period. Terbutaline and prenalterol infusions were followed by a dose-dependent increase of systolic blood pressure and heart rate. After placebo no effect on blood pressure or heart rate was seen. The study shows that CCK significantly enhances sigmoid motility in man and that selective beta-adrenergic agonists do not show any inhibitory influence on colonic motility stimulated with CCK. Since terbutaline inhibits sigmoid and rectal motility in man during rectal distention, it is suggested that the inhibitory effect of beta-2-adrenoceptor agonists may be dependent on the mode of background stimulation of the colon.
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