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(Circulation Research. 2003;93:893.)
© 2003 American Heart Association, Inc.

Editorials

The BK Channel

Protective or Detrimental in Genetic Hypertension?

Lucie H. Clapp, Rita I. Jabr

From BHF Laboratories, Department of Medicine, University College, London, UK.

Correspondence to Dr Lucie Clapp, BHF Laboratories, Department of Medicine, UCL, Rayne Building, 5 University St, London, WC1E 6JJ, UK. E-mail l.clapp@ucl.ac.uk

Key Words: Ca²⁺ sparks • potassium channels • electrophysiology • hypertension • vascular smooth muscle

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

Hypertension, or sustained elevation in systemic arterial blood pressure, is a major risk factor for diseases like stroke and myocardial infarction and affects around 25% of the adult population in the Western world.¹ The pathogenesis of hypertension is largely unknown, although clinical intervention with regimens to lower blood pressure (BP) significantly reduces morbidity and mortality associated with stroke.¹ Thus a considerable research effort has been directed toward elucidating the mechanisms controlling BP. In this issue of Circulation Research, Amberg and Santana² have put forward a novel concept that downregulation of the ß1 subunit of the large-conductance, Ca²⁺-activated K⁺ (BK) channel may be an integral component in the development of vascular dysfunction during genetically induced hypertension. To understand the implications of the present findings, we will first summarize the current concepts about the role of the BK channel in regulating vascular tone and its contribution to the pathogenesis of hypertension.

Regulation of Vascular Tone

Ca²⁺ influx through plasmalemmal voltage-dependent Ca²⁺ channels (VDCCs) is an important regulator of arterial tone in resistance vessels, the major determinant of BP.³ The open-state probability (P_o) of VDCCs is low around the resting membrane potential (Em), which in pressurized arteries ranges between -55 and -40 mV, and rises steeply with membrane depolarization. Thus, it is not surprising that agents influencing Em will have profound effects on blood vessel diameter. Indeed, opening of BK channels causes K⁺ efflux and membrane hyperpolarization, which underlies relaxation to a variety of endogenous vasodilators.⁴ Conversely, inhibition of K⁺ channels is commonly observed . . . [Full Text of this Article]

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