Propagation of vasodilation in resistance vessels of the hamster: development and review of a working hypothesis.

In many tissues, a substantial fraction of total vascular resistance resides in the feed arteries that give rise to the microcirculation. We have explored the thesis that control of tissue blood flow is integrated over several levels of the vascular network, including feed arteries and microvessels. In response to muscular contraction, feed arteries (resting diameter 100-125 microns) of hamster cremaster and gracilis muscles dilated by 20-25%. Acetylcholine applied to distal microvessels of the cremaster induced a dilation that ascended into feed arteries not having direct contact with acetylcholine. In the hamster cheek pouch, iontophoretic application of acetylcholine onto an arteriole (diameter 20-30 microns) triggered a vasodilation that propagated along the arteriole. Propagation was not dependent on blood flow, indicating that the dilator response was conducted along the vessel wall. We found that preventing diameter changes in an arteriole segment along the apparent conducting pathway did not block propagated vasodilation, indicating that propagation was not mediated by a myogenic mechanism requiring changes in smooth muscle length. We investigated whether the conduction of a vasodilatory stimulus may be mediated by either a neural plexus intrinsic to microvessels or cell-cell coupling between the cells composing the arteriole. Tetrodotoxin (10(-6) M) did not block propagated vasodilation, indicating that propagation is not mediated by a neural pathway. Hypertonic sucrose solution applied to an arteriole segment along the apparent conducting pathway attenuated propagation significantly, which is consistent with its reported effect to decouple gap junctions between cells. Thus, propagated vasodilation in arterioles may be mediated by direct cell-cell conduction.