A high salt diet has been shown to increase renal mass of intact rats, although the mechanism by which this occurs has not been investigated. We used Dahl rats that are sensitive (DS) or resistant (DR) to the hypertensinogenic effect of salt to examine changes in renal size and composition caused by a high salt diet. Renal index, deoxyribonudeic add (DNA), protein, water content, protein/DNA ratio, and cell number and size were measured in age-matched DR and DS on a high salt diet for 7,14, or 28 days. The results were compared with those obtained from respective rats on a low salt diet. High salt diet elevated renal index and protein hi DR and DS rats at each time point. After 7 days of a high salt diet, DNA increased in DS only. Protein/DNA ratio was progressively decreased by a high salt diet in DS and remained unchanged in DR rats. Cell number was increased 35% in DS versus only 13% in DR rats at 4 weeks. Cell size decreased 24% in DS and only 11% in DR rats. These results indicate that renal growth due to hyperplasia accompanies ingestion of a high salt diet in both DR and DS rats, but the rate of growth and the mechanism through which it occurs differ between strains. This difference may be important in delineating salt sensitivity and future development of hypertension. {Hypertension 1989;13:122-127) N umerous studies of renal enlargement have been conducted after reduction of renal mass. The mechanism by which compensatory renal growth occurs has been ascribed mainly to hypertrophy, 1 although a component of hyperplasia has been found in at least one study.2 Compensatory renal growth occurs independent of changes in blood pressure and many factors are known to modify its extent, including age, 3 hormones, 4 and diet. 5 We found only one published report of the effect of salt intake on renal growth in the absence of renal ablation.6 That study demonstrated increased renal mass after ingestion of a high salt diet by normal rats, but the mechanism of growth was not investigated. In order to gain further insight into this question, we have studied the effect of salt consumption on renal size and composition in Dahl rats Received August 29, 1988; accepted October 19, 1988. sensitive (DS) or resistant (DR) to the hypertensinogenic effect of salt. The data permit analysis of the degree to which renal growth on a high salt diet is due to hyperplasia or hypertrophy and the detection of differences between the two strains. Materials and MethodsMale DR and DS rats were obtained as 26-to 32-day-old weanlings from Brookhaven National Laboratories (Upton, New York), housed individually, and maintained on low salt chow containing 0.4% NaCl until introduction of high salt chow containing 8.0% NaCl. All animals in this study consumed standard rodent laboratory chow (5001, Purina Laboratories, Richmond, Indiana) with a protein content of 23% and a potassium content of 1.1%. The NaCl content of this chow was adjusted to yield either a low or high salt diet. Three experimental groups and one control group were designated...
Alterations in Na, K ATPase pump activity as well as erythrocyte (RBC) intracellular sodium concentration (Nai) have been demonstrated in humans and rats with established hypertension. The contribution of hypertension itself to these changes is unclear. Accordingly, we investigated RBC ion transport and plasma ouabain-like factor (OLF) in four- to five-week old normotensive Dahl salt-sensitive (DS) and salt-resistant (DR) rats on low salt diet. Although both strains were normotensive, systolic blood pressure (SBP) of DS (123 +/- 2 mm Hg) was higher than that of DR (116 +/- 1 mm Hg). No interstrain difference was evident in RBC pump activity measured as ouabain-sensitive 86rubidium (86Rb) uptake (DS = 0.277 +/- .030 and DR = 0.271 +/- .029 mumol/10(9)RBC/h) even though RBC Nai was greater in DS than DR (14.9 +/- 2.0 v 10.7 +/- 1.0 mEq/L; P less than 0.05). Plasma OLF was higher in DS than DR (28.9 +/- 4.7 v 16.5 +/- 2.3 pmol/mL; P less than 0.05), but did not correlate with RBC pump activity in either strain. RBC Nai was directly correlated with pump activity in DS (r = 0.84, P less than 0.01) and demonstrated a trend to correlate in DR (r = 0.71, P = 0.07). RBC Nai was also directly correlated with SBP in DR (r = 0.73, P less than 0.05) and DS (r = 0.70, P = 0.05). We conclude that RBC Nai is genetically determined in Dahl rats and is elevated in normotensive DS who are at risk for hypertension development.(ABSTRACT TRUNCATED AT 250 WORDS)
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