Remote arteriolar dilations in response to muscle contraction under capillaries

In hamster cremaster muscle, it has been shown previously that contraction of skeletal muscle fibers underlying small groups of capillaries (modules) induces dilations that are proportional to metabolic rate in the two arteri olar generations upstream of the stimulated capillaries (Berg BR, Cohen KD, and Sarelius IH. Am J Physiol Heart Circ Physiol 272: H2693-H2700, 1997). These remote dilations were hypothesized to be transmitted via gap junction s and not perivascular nerves. In the present study, halothane (0.07%) bloc ked dilation in the module inflow arteriole, and dilation in the second art eriolar generation upstream, the branch arteriole, was blocked by both 600 mosM sucrose and halothane but not tetrodotoxin (2 mu M). Dilations in both arterioles were not blocked by the gap junction uncoupler 18-beta-glycyrrh etinic acid (40 mu M), and 80 mM KCl did not block dilation of the module i nflow arteriole. These data implicate a gap junctional-mediated pathway ins ensitive to 18-beta-glycyrrhetinic acid in dilating the two arterioles upst ream of the capillary module during "remote'' muscle contraction. Dilation in the branch arteriole, but not the module inflow arteriole, was attenuate d by 100 mu M N-omega-nitro-L-arginine. Thus selective contraction of muscl e fibers underneath capillaries results in dilations in the upstream arteri oles that have characteristics consistent with a signal that is transmitted along the vessel wall through gap junctions, i.e., a conducted vasodilatio n. The observed insensitivities to 18-beta-glycyrrhetinic acid, to KCl, and to N-omega-nitro-L-arginine suggest, however, that there are multiple sign aling pathways by which remote dilations can be initiated in these microves sels.