The role of vagal adrenergic activity in the mechanism of gastric acid secretion after pylorus-ligation in the rat

Abstract

Abstract The role of the vagus nerve and adrenoceptor stimulation in acid secretion after pylorus-ligation in the rat has been examined. All drugs were administered intraperitoneally. Atropine (5 mg kg−1) depressed the H+ output (111 μmol ± 33·8 vs 412·5 μmol ± 62·2, mean ± s.e.m., n = 10, P<0·001); Cimetidine (40 mg kg−1) did not enhance this action, while vagotomy was more effective than atropine (32·7 μmol ± 4·9, mean ± s.e.m., n = 10, P<0·05). Atropine (10 mg kg−1) produced a similar depression to the 5 mg kg−1 dose. Cimetidine (100 mg kg−1) depressed the H+ output (248·5 μmol ± 46·8, mean ± s.e.m., n = 10, P<0·05). Propranolol (5–20 mg kg−1) had no significant effect on the H + output but dose-dependent inhibition was produced by phenoxybenzamine or phentolamine; an inhibition similar to that achieved by vagotomy was seen with the 20 mg kg−1 dose. Both these drugs (5 or 10 mg kg−1) had no significant effect on the H+ output when given with atropine (5 mg kg−1) but the H+ output was significantly lower than that produced by either drug at the same dose given alone. Atropine (5 mg kg−1) with phenoxybenzamine or phentolamine (20 mg kg−1) produced H + output not significantly different from that with vagotomy or either α-adrenoceptor given alone at 20 mg kg−1, but the result was significantly (P<0·05) lower than the H+ output with atropine (5 mg kg−1) alone. The results suggest that pylorus-ligation in the rat produces vagal α-adrenoceptor delivery to the stomach causing cholinergic and non-cholinergic stimulation to acid secretion.