Abstract
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) |
|---|---|
| Pages (from-to) | 607-611 |
| Number of pages | 5 |
| Journal | Nippon rinsho. Japanese journal of clinical medicine |
| Volume | 54 |
| Issue number | 3 |
| State | Published - Mar 1996 |
ASJC Scopus subject areas
- General Medicine