This Article Full Text Full Text (PDF) Correction Correction (v53,pe21) All Versions of this Article: 53/2/118    most recent HYPERTENSIONAHA.108.125310v2 HYPERTENSIONAHA.108.125310v1 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 PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Armando, I. Articles by Jose, P. A. Search for Related Content PubMed PubMed Citation Articles by Armando, I. Articles by Jose, P. A. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Dietary Sodium Related Collections Other hypertension Endothelium/vascular type/nitric oxide Related Article

(Hypertension. 2009;53:118.)
© 2009 American Heart Association, Inc.

Editorial Commentaries

Sensing Salt Intake

Ines Armando; Pedro A. Jose

From the Department of Pediatrics and Physiology and Biophysics, Georgetown University Medical Center, Washington, DC.

Correspondence to Ines Armando, PhD, Department of Pediatrics, Georgetown University Medical Center, 4000 Reservoir Rd NW, Washington, DC 20057. E-mail ma383@georgetown.edu

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

The long-term regulation of blood pressure rests on renal and nonrenal mechanisms and depends on a delicate balance between vasoconstrictor and vasodilator hormones and humoral agents, as well as those factors that act to increase or decrease renal sodium transport. Hypertension develops when this balance is disrupted and abnormalities in the regulation of ion transport intrinsic and extrinsic to the kidney have been proposed to cause essential hypertension. Pressure natriuresis is a key component in the regulation of body fluid volume. In all forms of hypertension, there is a shift of the renal pressure natriuresis curve that requires increased arterial pressure to maintain normal sodium and water balance.

The genetic causes of essential hypertension have been difficult to identify. More than one gene is undoubtedly involved because Mendelian dominant and recessive traits are not readily discernible in hypertensive subjects, except in those rare cases of monogenic hypertension. Moreover, in hypertensive persons, it is likely that risk-predisposing genes are engaged in a complex network of gene-gene and gene-environment interactions.^1,2

High salt (NaCl) consumption contributes to the development of hypertension and is considered to be an independent risk factor for vascular remodeling, cardiac hypertrophy, and stroke. Salt sensitivity is defined as a fall in blood pressure during salt restriction and a rise during salt repletion/supplementation.³ Salt sensitivity and resistance have a large variety of determinants, including genetic factors, race/ethnicity, age, body mass, and diet. Hypertension and salt sensitivity of blood pressure are 2 conditions of which the etiologies are still elusive because . . . [Full Text of this Article]

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