The pivotal role of renal vasodysfunction in salt sensitivity and the initiation of salt-induced hypertension

The pivotal role of renal vasodysfunction in salt sensitivity and the initiation of salt-induced... Purpose of reviewFor decades, it has been widely accepted that initiation of salt-induced hypertension involves a type of kidney dysfunction (natriuretic handicap), which causes salt-sensitive subjects to initially excrete less of a sodium load than normal subjects and undergo abnormal increases in cardiac output, and therefore blood pressure. Here we discuss emerging views that renal vasodysfunction, not natriuretic dysfunction (subnormal sodium excretion), is usually a critical factor initiating salt-induced hypertension.Recent findingsSerious logical issues have been raised with arguments supporting historical views that natriuretic dysfunction initiates hypertension in response to increased salt intake. Most salt-sensitive humans do not have a ‘natriuretic handicap’ causing them to excrete a sodium load more slowly and retain more of it than salt-resistant normal subjects. Mounting evidence indicates that in most salt-sensitive subjects, renal vasodysfunction, defined as impaired renal vasodilation and abnormally increased renal vascular resistance in response to increased salt intake, in the absence of greater sodium retention than in salt-loaded normal subjects, is involved in initiation of salt-induced hypertension.SummaryTo advance discovery, prevention, and treatment of primary abnormalities causing salt-induced hypertension, greater research emphasis should be placed on identifying mechanisms mediating subnormal renal vasodilation and abnormally increased renal vascular resistance in response to high-salt diets. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Opinion in Nephrology & Hypertension Wolters Kluwer Health

The pivotal role of renal vasodysfunction in salt sensitivity and the initiation of salt-induced hypertension

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Publisher
Wolters Kluwer Health
Copyright
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
ISSN
1062-4821
eISSN
1473-6543
D.O.I.
10.1097/MNH.0000000000000394
Publisher site
See Article on Publisher Site

Abstract

Purpose of reviewFor decades, it has been widely accepted that initiation of salt-induced hypertension involves a type of kidney dysfunction (natriuretic handicap), which causes salt-sensitive subjects to initially excrete less of a sodium load than normal subjects and undergo abnormal increases in cardiac output, and therefore blood pressure. Here we discuss emerging views that renal vasodysfunction, not natriuretic dysfunction (subnormal sodium excretion), is usually a critical factor initiating salt-induced hypertension.Recent findingsSerious logical issues have been raised with arguments supporting historical views that natriuretic dysfunction initiates hypertension in response to increased salt intake. Most salt-sensitive humans do not have a ‘natriuretic handicap’ causing them to excrete a sodium load more slowly and retain more of it than salt-resistant normal subjects. Mounting evidence indicates that in most salt-sensitive subjects, renal vasodysfunction, defined as impaired renal vasodilation and abnormally increased renal vascular resistance in response to increased salt intake, in the absence of greater sodium retention than in salt-loaded normal subjects, is involved in initiation of salt-induced hypertension.SummaryTo advance discovery, prevention, and treatment of primary abnormalities causing salt-induced hypertension, greater research emphasis should be placed on identifying mechanisms mediating subnormal renal vasodilation and abnormally increased renal vascular resistance in response to high-salt diets.

Journal

Current Opinion in Nephrology & HypertensionWolters Kluwer Health

Published: Mar 1, 2018

References

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