Effects of alpha‐adrenoceptor agonists and antagonists on duodenal surface epithelial HCO₃‐secretion in the ratin 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 HCO 3 ‐ by the surface epithelium was measured by continuous titration at luminal pH 7.40. Noradrenaline at doses of 25–200 μg kg ‐1 h ‐1 had no (net) effect on duodenal HCO 3 ‐ secretion while the non‐selective α‐adrenoceptor antagonist phentolamine (20–1000 μg 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 α 1 ,‐adrenoceptor agonist, phenylephrine (100 and 500 μg kg ‐1 h ‐1 ) stimulated HCO 3 ‐ secretion in a dose‐dependent manner and this response was abolished by the α 1 ‐adrenoceptor antagonist prazosin (0.5 mg kg ‐1 ) while the β‐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 α 2 ‐adrenoceptor agonist clonidine (0.75‐15.0 μg kg ‐1 ). The results thus strongly suggest that a,‐adrenoceptor stimulation increases while α 2 ‐adrenoceptor stimulation decreases duodenal surface epithelial HCO 3 ‐ ‐secretion. This might explain the absence of a net effect of noradrenaline.