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(Circulation Research. 2001;88:132.)
© 2001 American Heart Association, Inc.

Editorials

Potassium Ions as Vasodilators: Role of Inward Rectifier Potassium Channels

Delrae M. Eckman, Mark T. Nelson

From the Department of Pharmacology, University of Vermont College of Medicine, Burlington, Vt.

Correspondence to Mark T. Nelson, PhD, Department of Pharmacology, Given Building, B326, University of Vermont College of Medicine, Burlington, VT 05405. E-mail nelson@salus.med.uvm.edu

Key Words: kidney • afferent arteriole • potassium channels • renal arterioles

	Introduction

 
External potassium ions have long been known as mediators of vasodilation of several vascular beds, including the coronary and cerebral circulations.^{1 2 3 4 5 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 hyperpolarizing factor.⁸

Two targets of external potassium ions have been proposed: the Na⁺/K⁺ 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 Na⁺/K⁺ ATPase is activated by external potassium with a half-activation constant of about 1 to 2 mmol/L¹⁰ and saturation above 5 mmol/L.^{11 12} Activation of the Na⁺/K⁺ ATPase by elevating external potassium from nominally 0 to 5 mmol/L causes transient hyperpolarization and dilation⁵ ; the transient nature presumably reflects the extrusion of sodium until a new steady state is reached. In contrast, elevation of external potassium causes a graded shift in the apparent voltage-dependence of the inward rectifier potassium channel conductance,¹³ which can lead to a maintained hyperpolarization and dilation.¹⁴ Unfortunately, the dissection of these pathways until recently has relied on two imperfect pharmacological probes: cardiotonic steroids, such as ouabain, and barium ions. Inhibition of the Na⁺/K⁺ ATPase with ouabain leads to a membrane potential depolarization, an elevation . . . [Full Text of this Article]

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