Abstract

beta Adrenoceptor blockade is known to accelerate transit through the small intestine without changing either the number or pattern of intestinal contractions. This study therefore tested the hypothesis that an increase in intraluminal aboral propulsive force may contribute to this transit acceleration. Twenty paired studies were performed, in 10 healthy volunteers, after oral administration of either 100 mg atenolol (a selective beta 1 antagonist) or matched dummy tablets according to a double blind, randomised protocol. The frequency of occurrence of, and the propulsive force exerted by, traction events related to intestinal contractions were measured, using a combined traction force detector and manometry assembly. After atenolol, a consistent increase in the force generated per traction event was noted, both for propagating contractions mean (SEM) (12.0 (1.8) g v control 5.9 (0.07) g; p < 0.05) and for stationary (11.6 (1.4) g v control 7.0 (0.7) g; p < 0.05). In contrast no change in the number of traction events was noted (control v atenolol = 1.6 (0.3) v 1.64 (0.4) per min for propagating and 0.7 (0.1) v 0.85 (0.16) per min for stationary contraction; p > 0.05). beta Adrenoceptor blockade thus increases the propulsive force generated by intestinal contractions, possibly by removing a sympathetic neural inhibition of intestinal tone.