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.
|Original language||English (US)|
|Number of pages||5|
|Journal||Nippon rinsho. Japanese journal of clinical medicine|
|State||Published - Mar 1996|
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