The rapid onset of vasodilatation within seconds of a single contraction suggests that the vasodilators involved may be products of skeletal muscle activation, such as potassium (K(+)). To test the hypothesis that K(+) was in part responsible for the rapid dilatation produced by muscle contraction we stimulated four to five skeletal muscle fibres in the anaesthetized hamster cremaster preparation in situ and measured the change in diameter of arterioles at a site of overlap with the stimulated muscle fibres before and after a single contraction stimulated over a range of stimulus frequencies (4, 10, 20, 30, 40, 60 and 80 Hz; 250 ms train duration). Muscle fibres were stimulated in the absence and presence of an inhibitor of a source of K(+), the voltage dependent K(+) channel inhibitor 3,4-diaminopyridine (DAP, 3 x 10(-4) M) and inhibitors of the K(+) dilatory signal transduction pathway, either a Na(+) K(+)-ATPase inhibitor (ouabain; 10(-4) M) or an inward rectifying K(+) channel inhibitor (barium chloride, BaCl(2); 5 x 10(-5) M). We observed significant inhibitions of the rapid dilatation at all stimulus frequencies with each inhibitor. The dilatory event at 4 s was significantly inhibited at all stimulus frequencies by an average of 65.7 +/- 3.6%, 58.8 +/- 6.1% and 64.4 +/- 2.1% in the presence DAP, ouabain and BaCl(2), respectively. These levels of inhibition did not correlate with non-specific changes in force generation by skeletal muscle measured in vitro. Therefore, our data support that K(+) is involved in the rapid dilatation in response to a single muscle contraction across a wide range of stimulus frequencies.