Ms. Mozaffari et Jm. Wyss, Dietary NaCl-induced hypertension in uninephrectomized Wistar-Kyoto rats: Role of kidney function, J CARDIO PH, 33(5), 1999, pp. 814-821
Citations number
42
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
This study tests the hypothesis that combination of unilateral nephrectomy
and a high sodium chloride (NaCl) diet causes hypertension in otherwise nor
motensive Wistar-Kyoto (WKY) rats and that this hypertensive response is du
e to a deficit in the remaining kidney's function. Four-week-old male WKY r
ats underwent either a right nephrectomy or a sham operation. Two weeks lat
er, 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 parameter
s and renal excretory responses were measured, in the conscious animals, be
fore and after administration of a 30-min isotonic saline challenge (5% of
body weight). The high-NaCl diet increased arterial pressure in the unineph
rectomized but nor in sham-operated rats; the development of hypertension w
as associated with increases in baseline renal excretion of fluid and sodiu
m and diuretic and natriuretic responses to the isotonic saline challenge.
The increased diuresis and natriuresis in the hypertensive WKY rats were re
lated to a significant reduction in renal tubular reabsorption and an assoc
iated increase in fractional excretion of fluid and sodium. The high-NaCl d
iet 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 t
he normotensive WKY rats, but the hypertensive response is not likely due t
o a functional deficit in the remaining kidney.