AJP - Gastrointestinal and Liver Physiology, Vol 251, Issue 4 453-G459, Copyright © 1986 by American Physiological Society
Inhibitory effects of beta-adrenergic agonists on gastric acid secretion in dogs
M. H. Stevens, R. C. Thirlby, C. T. Richardson, M. A. Fredrickson, R. H. Unger and M. Feldman
We evaluated the effect of two beta-adrenergic agonists, isoproterenol
(nonselective agonist) and terbutaline (selective beta 2-agonist), on
gastric acid secretion stimulated by intravenous pentagastrin, bethanechol,
or histamine in dogs with gastric fistulas. Intravenous infusion of
isoproterenol or terbutaline inhibited pentagastrin-stimulated acid
secretion to a significantly greater extent than they inhibited
bethanechol- or histamine-stimulated acid secretion. For example,
isoproterenol (12 micrograms X kg-1 X h-1) reduced mean pentagastrin-,
bethanechol-, and histamine-stimulated acid output by 86, 63, and 14%,
respectively. Percent inhibition of acid secretion with terbutaline (30
micrograms X kg-1 X h-1) averaged 60, 17, and 24% for pentagastrin,
bethanechol, and histamine, respectively. Terbutaline also inhibited
pentagastrin-stimulated acid secretion from vagally denervated fundic
pouches in a dose-related manner. Plasma somatostatin-like immunoreactivity
was significantly higher during infusion of terbutaline plus pentagastrin
than during infusion of pentagastrin alone. However, an intravenous
infusion of 0.3 microgram X kg-1 X h-1 somatostatin-14 had no effect on
pentagastrin-stimulated acid secretion from the gastric fistula, even
though this infusion increased plasma somatostatin-like immunoreactivity to
the same extent as terbutaline plus pentagastrin infusion. Thus the amount
of somatostatin released during terbutaline infusion was not sufficient to
explain the inhibition of pentagastrin-stimulated acid secretion observed.
