Presynaptic inhibition of sympathetic fibers participating in vasodilatation in response to K+-induced contraction of frog skeletal muscle.

Experiments were performed on an autoperfused transparent frog muscle (m. cutaneus pectoris) with the purpose of elucidating possible mechanisms of functional hyperaemia. The diameter of a primary arteriole was followed before and after a K+-induced contracture lasting 20 s. The vasodilatation following this period of activity was expressed as the diameter change relative to the maximal possible diameter increase. The results emphasize adenosine as an important substance participating in vasodilatation in active skeletal muscle, its effect possibly being presynaptic (prejunctional) inhibition of sympathetic vasoconstrictor fibers to arteriolar smooth muscle (sympathetic uncoupling), in addition to the well-known direct effect (relaxation) on vascular smooth muscle cells. The presence of a strong resting sympathetic tone was demonstrated by local application of phentolamine (7.1 X 10(-5) M) that led to a large diameter increase. The purinoceptor blocking agent, 8-phenyltheophylline (8-PTP) invariably attenuated post-contraction vasodilatation, the adenosine transport inhibitor dipyridamole (10(-5) M) increased the hyperaemia response. Lack of sympathetic arteriolar tone during hyperaemia was demonstrated by the absence of a dilatory effect of phentolamine applied in the post-contraction period. Conversely, blockage of purinoceptors by 8-PTP during and after the contracture allowed sympathetic discharge to continue as verified by application of phentolamine, now leading to further vasodilatation. We suggest that presynaptic inhibition of sympathetic nerve endings by adenosine participates in vasodilatation in frog skeletal muscle.