Salt-sensitive hypertension, Na+/Ca2+ exchanger, and vascular smooth muscle.
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.
Iwamoto
Takahiro
T
Department of Pharmacology, School of Medicine, Fukuoka University, Jonan-ku, Fukuoka, Japan. tiwamoto@cis.fukuoka-u.ac.jp
Kita
Satomi
S
Katsuragi
Takeshi
T
D000814:Aniline Compounds / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D009119:Muscle Contraction / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D010647:Phenyl Ethers / Q000494:pharmacology / Q000627:therapeutic use; D012982:Sodium, Dietary / Q000494:pharmacology; D019831:Sodium-Calcium Exchanger / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000502:physiology*
D000814:Aniline Compounds; D010647:Phenyl Ethers; C430918:SEA 0400; D012982:Sodium, Dietary; D019831:Sodium-Calcium Exchanger; C110374:sodium-calcium exchanger 1