External potassium ions have long been known asmediators of vasodilation of several vascular beds,including the coronary and cerebral circulations.1–6 Indeed, potassium ions have been viewed as communicators of the metabolic state of the cells that surround blood vessels. For example, release of potassium ions from neurons is communicated through glial cells to regulate cerebral artery diameter.7 Recently, it has been suggested that the potassium ions from endothelial cells may signal smooth muscle to relax and, as such, may constitute an endothelial-derived hyperpo-larizing factor.8 Two targets of external potassium ions have been pro-posed: the Na1/K1 ATPase and the inward rectifier potassium channel.1,5,9 An elevation of external potassium causes very different responses of these two molecular targets. The electrogenic Na1/K1 ATPase is activated by external potas-sium with a half-activation constant of about 1 to 2 mmol/L10