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(Circulation Research. 2007;101:959.)
© 2007 American Heart Association, Inc.

Editorials

Local Sodium, Global Reach

Filling the Gap Between Salt and Hypertension

Mordecai P. Blaustein, W. Gil Wier

From the Departments of Physiology (M.P.B., W.G.W.) and Medicine (M.P.B.) and the Center for Heart, Hypertension, and Kidney Disease (M.P.B., W.G.W.), University of Maryland School of Medicine, Baltimore, Md.

Correspondence to Mordecai P. Blaustein, MD, Department of Physiology, University of Maryland School of Medicine, 655 W. Baltimore Street, Baltimore, MD 21201. E-mail mblaustein@som.umaryland.edu

See related article, pages 1030–1038

Key Words: sodium • subplasma membrane microdomains • TRPC6 • receptor-operated channels • Na⁺/Ca²⁺ exchanger

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

The plasma membrane (PM) Na⁺/Ca²⁺ exchanger (NCX) in vascular smooth muscle is an unique link between the trans-PM Na⁺ electrochemical gradient and intracellular Ca²⁺ and, therefore, between Na⁺ ions and Ca²⁺ signaling, vascular tone and blood pressure.¹ The mechanisms by which Na⁺ normally enters the myocytes and influences the Na⁺ gradient and NCX activity are, however, incompletely understood. Our view of how Na⁺ ions help regulate sarco-/endoplasmic reticulum (S/ER) Ca²⁺ stores and contractility in arteries has now been signally enhanced by Poburko and colleagues.² Using CoroNa green, a Na⁺-sensitive fluorochrome, they observed local Na⁺ concentration transient increases ("LNats") in cultured arterial myocytes. The LNats were generated by Na⁺ entry through cation-selective TRPC6 channels, a member of the TRP (transient receptor potential) channel family.² This is direct, dynamic evidence for a predicted sub-PM compartment with greatly restricted Na⁺ diffusion^3,4 in which the local rise in Na⁺ concentration should drive Ca²⁺ into the myocytes via NCX.

The present study has broad implications for Ca²⁺ homeostasis and signaling. Earlier vascular smooth muscle studies indicated that other members of the TRP channel family might also admit Na⁺ to sub-PM domains.^3,5 Indirect evidence,⁶ as well as an electron microprobe study, indicate that cardiomyocytes, too, can exhibit elevated local sub-PM Na⁺ concentrations ([Na⁺]_SPM).⁷ Moreover, comparable diffusion-restricted, sub-PM cytosolic compartments may also be present in other types of cells (e.g., astrocytes⁸).

To explain how S/ER Ca²⁺ stores in smooth muscles could refill from the extracellular fluid without inducing contractions,^9,10 van Breeman and . . . [Full Text of this Article]

Related Article:

Transient Receptor Potential Channel 6–Mediated, Localized Cytosolic [Na⁺] Transients Drive Na⁺/Ca²⁺ Exchanger–Mediated Ca²⁺ Entry in Purinergically Stimulated Aorta Smooth Muscle Cells

Damon Poburko, Chiu-Hsiang Liao, Virginia S. Lemos, Eric Lin, Yoshiaki Maruyama, William C. Cole, and Cornelis van Breemen
Circ. Res. 2007 101: 1030-1038. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				M. P. Blaustein, J. Zhang, L. Chen, H. Song, H. Raina, S. P. Kinsey, M. Izuka, T. Iwamoto, M. I. Kotlikoff, J. B. Lingrel, et al. The Pump, the Exchanger, and Endogenous Ouabain: Signaling Mechanisms That Link Salt Retention to Hypertension Hypertension, February 1, 2009; 53(2): 291 - 298. [Full Text] [PDF]