Abstract Redundancy, in active hyperaemia, where one vasodilator can compensate for another if the first is missing, would require that one vasodilator inhibits the effects of another, therefore if the first vasodilator is inhibited, its inhibitory influence on the second vasodilator is removed and the second vasodilator exerts a greater vasodilatory effect. We sought to test if vasodilators relevant to skeletal muscle contraction, (potassium (K+), adenosine (ADO) and nitric oxide (NO)) inhibit one another and, further, investigate the mechanisms for this interaction. We used the hamster cremaster muscle and intravital microscopy to directly visualize 2A arterioles when exposed to a range of concentrations of one vasodilator (10−8M‐10−5 M SNAP, 10−8M‐10−5 M ADO, 10 and 20 mm KCl) in the absence and then in the presence of a second vasodilator (10−7 M ADO, 10−7 M SNAP, 10 mm KCl). We found that KCl significantly attenuated SNAP‐induced vasodilatations by ∼65.8% and vasodilatations induced by 10−8M‐10−6 M ADO by ∼72.8%. Further, we observed that inhibition of KCl vasodilatation, by antagonizing either Na+/K+ATPase using ouabain or KIR channels using barium chloride, could restore the SNAP‐induced vasodilatation by up to ∼53.9% and 30.6% respectively, and restore the ADO‐induced vasodilatations by up to ∼107% and 76.7% respectively. Our data show that vasodilators relevant to muscle contraction can interact in a way that alters eachothers vasodilatory effectiveness. These data suggest that active hyperaemia may be the result of complex interactions between multiple vasodilators through a redundant control paradigm. This article is protected by copyright. All rights reserved