Acetylcholine activates a regenerative vasodilator mechanism that is sensitive to nitric oxide production.

Introduction: The conduction of changes in the diameter of arterioles plays an important role in the coordination of the blood flow distribution. The endothelium regulates vasomotor tone by generation of vasodilator signals, such as nitric oxide (NO) and endothelium-derived hyperpolarization (EDH). Endothelium-mediated vasodilator responses initiated in an arteriolar segment are conducted along the vessel length, which depends on the electrotonic spread of EDH signaling activated at the stimulation site, but, in contrast, the contribution of NO is controversial. Methods: We used the mouse cremaster muscle microcirculation Results: The response to ACh spread along the entire vessel showing only a slight decay and, in contrast, the dilation evoked by SNAP was restricted to the stimulation site, independently of the magnitude of the response. Blockade of NO production with 100 μM N Conclusion: These results suggest that ACh activates an NO sensitive mechanism of regenerative propagation of vasodilator responses, which contributes to our understanding of microvascular function and the complex integration of endothelial signaling pathways in the coordination of the blood flow distribution.