The pivotal role of renal vasodysfunction in salt sensitivity and the initiation of salt-induced hypertension
Language English Country Great Britain, England Media print
Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review
- MeSH
- Vascular Resistance * MeSH
- Hypertension etiology physiopathology MeSH
- Blood Pressure MeSH
- Sodium Chloride, Dietary adverse effects metabolism MeSH
- Kidney blood supply physiopathology MeSH
- Humans MeSH
- Vasodilation * MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Research Support, N.I.H., Extramural MeSH
- Names of Substances
- Sodium Chloride, Dietary MeSH
PURPOSE OF REVIEW: For 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 FINDINGS: Serious 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. SUMMARY: To 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.
Department of Laboratory Medicine UCSF School of Medicine San Francisco California
Department of Medicine UCSF School of Medicine San Francisco California USA
Institute of Physiology of the Czech Academy of Sciences Prague Czech Republic
References provided by Crossref.org
Mechanism-based strategies to prevent salt sensitivity and salt-induced hypertension