Salt-sensitive hypertension, Na+/Ca2+ exchanger, and vascular smooth muscle.

Abstract

Hypertension is the most common chronic disease and is the leading risk factor for death caused by stroke, myocardial infarction, and end-stage renal failure. The critical importance of excess salt intake in the pathogenesis of hypertension is widely recognized. However, the molecular mechanisms underlying salt-sensitive hypertension remain obscure. Recent studies using selective Na(+)/Ca(2+) exchanger (NCX) inhibitors and genetically engineered mice provide compelling evidence that salt-sensitive hypertension is triggered by Ca(2+) entry through NCX type 1 (NCX1) in arterial smooth muscle. Cardiotonic steroids, such as endogenous ouabain, which may contribute to the pathogenesis of salt-sensitive hypertension, seem to be necessary for NCX1-mediated hypertension. These findings have enabled us to explain how high salt intake leads to hypertension and further to describe the potential of vascular NCX1 as a new therapeutic or diagnostic target for salt-sensitive hypertension.

• Authors: Takahiro Iwamoto, Satomi Kita, Takeshi Katsuragi
• Journal: Trends in cardiovascular medicine (Trends Cardiovasc Med) Vol. 15 Issue 8 Pg. 273-7 (Nov 2005) ISSN: 1050-1738 [Print] United States
• PMID: 16297763 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Aniline Compounds
• Phenyl Ethers
• SEA 0400
• Sodium, Dietary
• Sodium-Calcium Exchanger
• sodium-calcium exchanger 1

Topics

• Aniline Compounds (pharmacology, therapeutic use)
• Animals
• Humans
• Hypertension (drug therapy, physiopathology)
• Muscle Contraction (physiology)
• Muscle, Smooth, Vascular (physiopathology)
• Phenyl Ethers (pharmacology, therapeutic use)
• Sodium, Dietary (pharmacology)
• Sodium-Calcium Exchanger (antagonists & inhibitors, metabolism, physiology)