Effects of alpha-adrenoceptor agonists and antagonists on duodenal surface epithelial HCO3-secretion in the rat in vivo.

In anesthetized rats a 12 mm segment of duodenum, distal to the Brunner's gland area and devoid of pancreatic and bile secretions, was cannulated in situ. Secretion of HCO3- by the surface epithelium was measured by continuous titration at luminal pH 7.40. Noradrenaline at doses of 25-200 micrograms kg-1 h-1 had no (net) effect on duodenal HCO3- secretion while the non-selective alpha-adrenoceptor antagonist phentolamine (20-1000 micrograms kg-1 intravenously) dose-dependently increased secretion. The phentolamine-induced rise in alkaline secretion was partially inhibited by noradrenaline but this effect was transient and was followed by an increase in secretion in spite of continuous infusion of noradrenaline. The alpha 1-adrenoceptor agonist, phenylephrine (100 and 500 micrograms kg-1 h-1) stimulated HCO3- secretion in a dose-dependent manner and this response was abolished by the alpha 1-adrenoceptor antagonist prazosin (0.5 mg kg-1) while the beta-adrenoceptor antagonist propranolol (1 mg kg-1) was without effect. Basal secretion, as well as secretion stimulated by phentolamine and/or phenylephrine, was inhibited by the alpha 2-adrenoceptor agonist clonidine (0.75-15.0 micrograms kg-1). The results thus strongly suggest that alpha 1-adrenoceptor stimulation increases while alpha 2-adrenoceptor stimulation decreases duodenal surface epithelial HCO3(-)-secretion. This might explain the absence of a net effect of noradrenaline.