FLOW-DEPENDENT REGULATION OF ARTERIOLAR DIAMETER IN RAT SKELETAL-MUSCLE IN-SITU - ROLE OF ENDOTHELIUM-DERIVED RELAXING FACTOR AND PROSTANOIDS

1. Arteriolar diameter in the resting rat spinotrapezius muscle was st udied by intravital video microscopy before and after blockade of the L-arginine-EDRF ((N-G-nitro-L-arginine, L-NNA) or the cyclo-oxygenase- prostacyclin (indomethacin) pathway. Blockade of either pathway leads to a decrease of arteriolar diameter of 25-40%, while the combined blo ckade of both results in vasoconstriction of 50-60%. 2. Alteration of blood flow velocity elicited by partial micropipette occlusion induces corresponding changes of vessel diameter. The flow-dependent diameter response is reduced by about 80% by L-NNA. By contrast, blockade of p rostanoid production shows no significant influence on vessel response to blood flow alteration in the range tested. 3. Transient overshooti ng vasodilatation is seen for about 1 min following the sudden restora tion of flow velocity subsequent to occlusion. In contrast to the init ial phase of this response, the late phase is blocked by L-NNA. 4. The findings suggest that basal release of endothelium-derived relaxing f actor (EDRF) and prostanoids leads to additive and independent dilator effects, and that flow-dependent diameter changes are primarily media ted by EDRF. 5. If present data are compared with literature reports, it appears that arterial flow sensitivity is most pronounced in the sm allest vessels. In such vessels, flow-dependent dilatation will amplif y even small changes of volume flow by more than four times.