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(Circulation Research. 2006;99:13.)
© 2006 American Heart Association, Inc.

Editorials

Molecular Coding of Kv1 Channels to Oppose Myogenic Constriction

Stephen V. Straub, Mark T. Nelson

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

Correspondence to Mark T. Nelson, Department of Pharmacology, University of Vermont, Given Building, Room B-333, 89 Beaumont Avenue, Burlington VT 05405-0068. E-mail Mark.Nelson@uvm.edu

See related article, pages 53–60

Key Words: voltage-gated potassium channel • myogenic response • vascular smooth muscle • cerebral circulation • Kv1 channel

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Resistance arteries possess an intrinsic ability to constrict in response to increased intraluminal pressure, the "myogenic response."¹ The ability of resistance vessels to modulate their diameter in response to changes in intraluminal pressure is thought to be an important component of blood flow autoregulation, such that constant blood flow and tissue perfusion are maintained in the face of variations in blood pressure.^2,3 Specifically, intraluminal pressure results in a graded smooth muscle cell (SMC) depolarization from about –65 mV to about –40 mV,⁴ likely because of activation of nonselective cation channels.⁵ This depolarization activates L-type voltage-dependent calcium (Ca²⁺) channels, leading to elevation of the SMC cytosolic Ca²⁺ concentration, SMC contraction, and vasoconstriction.⁶ In the absence of negative feedback mechanisms to oppose myogenic constriction, resistance arteries would likely exhibit unstable membrane potentials and fluctuations in vascular diameter as a result of Ca²⁺ dependent action potentials.⁷ However, in vivo, graded and sustained changes in vascular diameter occur, such that blood flow is maintained despite changes in pressure.¹ Activation of hyperpolarizing potassium (K⁺) conductances, which oppose depolarization and vasoconstriction, are critical negative feedback mechanisms responsible for controlling the extent of myogenic constriction.^2,3,8–10

Smooth muscle cells express two types of K⁺ channels which are primarily responsible for opposing myogenic depolarization: (1) the large conductance Ca²⁺ sensitive K⁺ (BK) channel, which is activated by both membrane depolarization and intracellular Ca²⁺,^8,11 and (2) voltage-gated K⁺ channels (K_V channels), which are steeply activated by membrane potential (V_m) depolarization.^9,10,12,13 Interestingly, BK channels appear to . . . [Full Text of this Article]