Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 293, Issue 4, Pages H2039-H2053Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00325.2007
Keywords
sodium; chloride; osmolality; plasma; tubular fluid; cerebrospinal fluid; salt intake
Funding
- NINDS NIH HHS [R21 NS052516] Funding Source: Medline
Ask authors/readers for more resources
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 mechano-sensitive, 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available