Dilatory responses of the isolated intestinal vasculature of the rat have been studied during constant infusion of acetylcholine (Ach), isoproterenol (IP) andmyotropic, i.e. Ca++ antagonistically acting doses of propranolol. The initial vasodilation was followed by a succeeding increase of flow resistance. This effect, called ‘escape phenomenon’ could constantly be proved during application of Ach, was dosedependent and reached a maximal escape quotient of nearly 30%. Large vasoconstrictive doses of Ach also showed an escape phenomenon indicating the probability of one basal mechanism causing the escape from vasodilation and vasoconstriction. Vasodilations evoked by infusion of IP and large doses of β-blockers showed escape reactions only in some cases. The discrepancy between the different escape behaviour can be understood by comparing the rate of development of the initial vasodilation, which was two times slower for IP and propranolol than for Ach. The escape from Ach-elicited vasodilations could be clearly reduced by myotropic acting doses of LB 46. These results demonstrate that the escape from vasodilation is not a drug-specific phenomenon but is of myogenic origin. The analogy of the escape from vasodilation and vasoconstriction suggests a common basal myogenic mechanism perhaps due to changes of Ca++-fluxes. Thus, the initial vascular reaction would represent an ‘overshoot’ and the escape an adjustment reaction in a ‘steady-state system’.