Renal sodium handling in ouabain-hypertensive rats / 中国医学科学院学报

ABSTRACT

<p><b>OBJECTIVE</b>To investigate renal sodium handling of ouabain-hypertensive rats and the role of renal sodium handling in pathogenesis of hypertension using endogenous trace lithium as a marker of proximal sodium reabsorption.</p><p><b>METHODS</b>Forty male Sprague-Dawley (SD) rats weighting 180-220 g were equally divided into normal control group and ouabain group randomly. Rats were infused with normal saline 1 ml/ (kg x d) or ouabain 27.8 microg/ (kg-d) intraperitoneally once a day respectively. Systolic blood pressure (SBP) and body weight were recorded weekly. Rats were sacrificed after 2 and 6 weeks respectively. Blood and 24 hour urine sample were collected to measure the serum and urinary concentration of sodium, potassium, trace lithium, and creatinine. Endogenous creatinine clearance rate (Ccr), fractional excretions of sodium (FE(Na)), and fractional excretions of lithium (FE(Li)), the ratios of urinary lithium to sodium (U(Li)/U(Na)), the ratios of urinary potassium to sodium (U(K)/U(Na)), and fractional reabsorption of sodium in the postproximal tubules (FDR(Na)) were also calculated. All were studied on their normal diet and ate salt freely.</p><p><b>RESULTS</b>Blood pressure had no significant difference in these two groups after 2 weeks (P > 0.05); After 4 weeks, however, blood pressure was significantly higher in ouabain group than in control group (P < 0.01). Body weight of rats had no significant difference during the experiment period (P > 0.05). Ccr and FE(Na) were similar in these 2 groups (P > 0.05). FE(Li), U(Li)/U(Na), U(K)/U(Na), and FDR(Na) of ouabain group were significantly lower than control group after 2 and 6 weeks (P < 0.05, P < 0.01, P < 0.001 respectively).</p><p><b>CONCLUSION</b>The reabsorption of sodium increases in the proximal tubule in ouabain-hypertensive rats, and such increase occurs before the development of hypertension. Therefore, increase of proximal reabsorption of sodium may be involved in the pathogenesis of ouabain-induced hypertension.</p>