Dietary NaCl-induced hypertension in uninephrectomized Wistar-Kyoto rats: role of kidney function.

This study tests the hypothesis that combination of unilateral nephrectomy and a high sodium chloride (NaCl) diet causes hypertension in otherwise normotensive Wistar-Kyoto (WKY) rats and that this hypertensive response is due to a deficit in the remaining kidney's function. Four-week-old male WKY rats underwent either a right nephrectomy or a sham operation. Two weeks later, the groups either were switched to a high (8%) NaCl diet or remained on the basal (0.72%) NaCl diet. At ages 3 and 6 months, hemodynamic parameters and renal excretory responses were measured, in the conscious animals, before and after administration of a 30-min isotonic saline challenge (5% of body weight). The high-NaCl diet increased arterial pressure in the uninephrectomized but not in sham-operated rats; the development of hypertension was associated with increases in baseline renal excretion of fluid and sodium and diuretic and natriuretic responses to the isotonic saline challenge. The increased diuresis and natriuresis in the hypertensive WKY rats were related to a significant reduction in renal tubular reabsorption and an associated increase in fractional excretion of fluid and sodium. The high-NaCl diet also increased renal excretion of fluid and sodium in the sham-operated rats; however, the uninephrectomized animals excreted much more fluid and sodium than did sham-operated rats. These data suggest that the combination of unilateral nephrectomy and dietary NaCl excess causes hypertension in the normotensive WKY rats, but the hypertensive response is not likely due to a functional deficit in the remaining kidney.