[Na+/H+ exchanger].
Recent investigations have revealed that an enhancement of Na+/H+ exchange activity is a frequently observed ion transport abnormality in hypertensive patients. To test the hypothesis that increased Na+/H+ exchange causes hypertension, we produced transgenic mice overexpressing Na+/H+ exchanger and analyzed their Na+ metabolism and blood pressure. Urinary excretion of water and Na+ was significantly decreased in transgenic mice and systolic blood pressure was elevated after salt loading. The impaired Na+ excretion suggested that the Na+/H+ exchanger overexpressed in the renal tubules increased Na+ reabsorption, which caused a blood pressure elevation by Na+ retention after excessive salt intake. Our results demonstrate that overexpression of Na+/H+ exchanger can be a genetic factor for salt-sensitive hypertension.
National Institute of Neuroscience, NCNP, Japan.
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Kuro-o
D000818:Animals; D006801:Humans; D006973:Hypertension / Q000209:etiology; D051379:Mice; D008822:Mice, Transgenic; D012964:Sodium / Q000378:metabolism; D017923:Sodium-Hydrogen Exchangers / Q000737:chemistry / Q000378:metabolism / Q000502:physiology
D017923:Sodium-Hydrogen Exchangers; D012964:Sodium