HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/4/H2039    most recent 00325.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (13) Citing Articles via Google Scholar Google Scholar Articles by Orlov, S. N. Articles by Mongin, A. A. Search for Related Content PubMed PubMed Citation Articles by Orlov, S. N. Articles by Mongin, A. A.

INVITED REVIEW

Salt-sensing mechanisms in blood pressure regulation and hypertension

¹Department of Medicine and Centre Hospitalier de l'Université de Montréal, Montreal, Quebec, Canada; and ²Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, New York

High salt consumption contributes to the development of hypertension and is considered an independent risk factor for vascular remodeling, cardiac hypertrophy, and stroke incidence. In this review, we discuss the molecular origins of primary sensors involved in the phenomenon of salt sensitivity. Based on the analysis of literature data, we conclude that the kidneys and central nervous system (CNS) are two major sites for salt sensing via several distinct mechanisms: 1) [Cl^–] sensing in renal tubular fluids, primarily by Na⁺-K⁺-Cl^– cotransporter (NKCC) isoforms NKCC2B and NKCC2A, whose expression is mainly limited to macula densa cells; 2) [Na⁺] sensing in cerebrospinal fluid (CSF) by a novel isoform of Na⁺ channels, Na_x, expressed in subfornical organs; 3) sensing of CSF osmolality by mechanosensitive, nonselective cation channels (transient receptor potential vanilloid type 1 channels), expressed in neuronal cells of supraoptic and paraventricular nuclei; and 4) osmolarity sensing by volume-regulated anion channels in glial cells of supraoptic and paraventricular nuclei. Such multiplicity of salt-sensing mechanisms likely explains the differential effects of Na⁺ and Cl^– loading on the long-term maintenance of elevated blood pressure that is documented in experimental models of salt-sensitive hypertension.

sodium; chloride; osmolality; plasma; tubular fluid; cerebrospinal fluid; salt intake

This article has been cited by other articles:

				J. C. Geerling and A. D. Loewy Aldosterone in the brain Am J Physiol Renal Physiol, September 1, 2009; 297(3): F559 - F576. [Abstract] [Full Text] [PDF]

				A. Y. Bagrov, J. I. Shapiro, and O. V. Fedorova Endogenous Cardiotonic Steroids: Physiology, Pharmacology, and Novel Therapeutic Targets Pharmacol. Rev., March 1, 2009; 61(1): 9 - 38. [Abstract] [Full Text] [PDF]

				F. Gao, D. Sui, R. M. Garavito, R. M. Worden, and D. H. Wang Salt Intake Augments Hypotensive Effects of Transient Receptor Potential Vanilloid 4: Functional Significance and Implication Hypertension, February 1, 2009; 53(2): 228 - 235. [Abstract] [Full Text] [PDF]