Stimulation of bicarbonate secretion by atypical beta-receptor agonists in rat cecum in vitro.

This study examined the effects of beta-adrenoceptor agonists on bicarbonate secretion by the rat cecum in vitro. Isoprenaline, the beta 2-selective agonist salbutamol and the 'atypical' beta-agonist SR58611A stimulated bicarbonate secretion in a concentration related manner. Another atypical agonist, BRL 37344, also stimulated. Responses to isoprenaline were antagonised by alprenolol and propranolol (both 20 microM) but not the selective antagonists practolol (10 microM) or ICI 1185511 (1 microM). Responses to SR 58611A were only antagonised by alprenolol. Replacement of Cl- by NO3- on the mucosal surface reduced basal secretion and abolished the response to isoprenaline. Exposure to a single concentration of atypical agonist resulted in desensitisation to a second application and to isoprenaline. There was no evidence of desensitisation with isoprenaline or salbutamol. The results show that beta-adrenoceptor agonists stimulated bicarbonate secretion in contrast to the previously described inhibitory effect of cholinergic drugs in this tissue. Stimulation was mediated by beta-adrenoreceptors, which had properties consistent with the atypical receptors described in gut smooth muscle and in adipose tissue. Both adrenergic and cholinergic drugs may act on the same mechanism of secretion which may involve an exchange of HCO3- for mucosal Cl-.