Ascending dilations are attributed to the conduction of hyper-polarizations via gap junctions. Since dilations span larger distances than can be explained by electrotonic conduction the signal must be amplified. We studied mechanisms that contribute to the conduction of dilations induced by adenosine (Ado) and acetylcholine (ACh).

ACh and Ado were applied via micropipettes and dilator responses were assessed at local and distant sites by intravital microscopy in the mouse cremaster muscle.

Local (and remote) dilations to ACh were abrogated by blockade of K_Ca-channels (charybdotoxin, 53% vs. 10%), whereas Ado-dilations were abolished by the K_ATP blocker glibenclamide (53% vs. 1%). Bupivacaine, a blocker of K- and Na-channels abrogated conducted dilations induced by Ado without altering the conduction if ACh was applied. However, neural pathways are not involved since mepivacaine was without effect. Blockade of K_V (4-AP) reduced only remote ACh dilations (1100 mm) from 52% to 20%. In contrast, remote Ado-dilations were reduced by blockade of K_IR-channels (Ba2+,75mM: 30% vs. 10%).

We conclude that local hyperpolarizations initiated by activation of K_Ca- (ACh) or K_ATP-channels (Ado) induce conducted dila-tions. Although a hyperpolarization seems to be the common de-nominator, the signal is amplified by different mechanisms.