A role for β‐adrenoreceptors in conducted vasodilation

The endothelium acts as the conduit for the intercellular spread of hyperpolarization and subsequent dilation over significant distances in small arteries and arterioles. In vascular tissue, β‐adrenoreceptors (ARs) activate K ATP channels leading to smooth muscle hyperpolarization. We investigated whether this hyperpolarization could lead to conducted dilation in rat isolated small mesenteric arteries. Both contraction and dilation to norepinephrine or epinephrine were insensitive to the K ATP channel blocker glibenclamide, despite fully blocking hyperpolarization to β‐AR stimulation. Focal application of epinephrine in pressurized arteries caused local vasoconstriction, while in precontracted arteries it additionally caused spreading vasodilatation. β‐AR stimulation evoked spreading dilatation that was endothelium‐dependent and inhibited by glibenclamide. Acetylcholine also evoked local and spreading dilatation that in contrast was insensitive to glibenclamide. These results demonstrate that β‐ARs can evoke spreading dilatation that depends on activation of K ATP channels. Supported by the Welcome Trust and British Heart Foundation.