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Impaired sodium excretion and salt-sensitive hypertension in corin-deficient mice.

Wang W, Shen J, Cui Y, Jiang J, Chen S, Peng J, Wu Q - Kidney Int. (2012)

Bottom Line: In the knockout mice on the high-salt diet there was an impairment of urinary sodium excretion and an increase in body weight, but no elevation of plasma renin or serum aldosterone levels.When the knockout mice on the high-salt diet were treated with amiloride, an epithelial sodium channel blocker that inhibits renal sodium reabsorption, the impaired urinary sodium excretion and increased body weight were normalized.Amiloride treatment also reduced high blood pressure caused by the high-salt diet in these mice.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Cardiology, Nephrology and Hypertension, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA.

ABSTRACT
Corin is a protease that activates atrial natriuretic peptide, a cardiac hormone important in the control of blood pressure and salt-water balance. Here we examined the role of corin in regulating blood pressure and sodium homeostasis upon dietary salt challenge. Radiotelemetry-tracked blood pressure in corin knockout mice on a high-salt diet (4% sodium chloride) was significantly increased; however, there was no such change in similarly treated wild-type mice. In the knockout mice on the high-salt diet there was an impairment of urinary sodium excretion and an increase in body weight, but no elevation of plasma renin or serum aldosterone levels. When the knockout mice on the high-salt diet were treated with amiloride, an epithelial sodium channel blocker that inhibits renal sodium reabsorption, the impaired urinary sodium excretion and increased body weight were normalized. Amiloride treatment also reduced high blood pressure caused by the high-salt diet in these mice. Thus, the lack of corin in mice impairs their adaptive renal response to high dietary salt, suggesting that corin deficiency may represent an important mechanism underlying salt-sensitive hypertension.

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Increased body weight in Cor−/− mice on high salt dietWT and Cor−/− mice were on 4% NaCl (a) or 0.3% NaCl (b) diets. Body weight changes up to 3 weeks were examined. n=5 per group. P values vs. WT of the same group by two-way ANOVA were shown. n.s., not statistically significant.
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Figure 3: Increased body weight in Cor−/− mice on high salt dietWT and Cor−/− mice were on 4% NaCl (a) or 0.3% NaCl (b) diets. Body weight changes up to 3 weeks were examined. n=5 per group. P values vs. WT of the same group by two-way ANOVA were shown. n.s., not statistically significant.

Mentions: In Cor−/− mice on the high-salt diet, the impaired urinary Na+/Cl− excretion was accompanied with increased body weight compared to that in WT mice (Figure 3a). Such a difference in body weight gain between WT and Cor−/− mice was not observed on the normal salt diet (Figure 3b).


Impaired sodium excretion and salt-sensitive hypertension in corin-deficient mice.

Wang W, Shen J, Cui Y, Jiang J, Chen S, Peng J, Wu Q - Kidney Int. (2012)

Increased body weight in Cor−/− mice on high salt dietWT and Cor−/− mice were on 4% NaCl (a) or 0.3% NaCl (b) diets. Body weight changes up to 3 weeks were examined. n=5 per group. P values vs. WT of the same group by two-way ANOVA were shown. n.s., not statistically significant.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3376235&req=5

Figure 3: Increased body weight in Cor−/− mice on high salt dietWT and Cor−/− mice were on 4% NaCl (a) or 0.3% NaCl (b) diets. Body weight changes up to 3 weeks were examined. n=5 per group. P values vs. WT of the same group by two-way ANOVA were shown. n.s., not statistically significant.
Mentions: In Cor−/− mice on the high-salt diet, the impaired urinary Na+/Cl− excretion was accompanied with increased body weight compared to that in WT mice (Figure 3a). Such a difference in body weight gain between WT and Cor−/− mice was not observed on the normal salt diet (Figure 3b).

Bottom Line: In the knockout mice on the high-salt diet there was an impairment of urinary sodium excretion and an increase in body weight, but no elevation of plasma renin or serum aldosterone levels.When the knockout mice on the high-salt diet were treated with amiloride, an epithelial sodium channel blocker that inhibits renal sodium reabsorption, the impaired urinary sodium excretion and increased body weight were normalized.Amiloride treatment also reduced high blood pressure caused by the high-salt diet in these mice.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Cardiology, Nephrology and Hypertension, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA.

ABSTRACT
Corin is a protease that activates atrial natriuretic peptide, a cardiac hormone important in the control of blood pressure and salt-water balance. Here we examined the role of corin in regulating blood pressure and sodium homeostasis upon dietary salt challenge. Radiotelemetry-tracked blood pressure in corin knockout mice on a high-salt diet (4% sodium chloride) was significantly increased; however, there was no such change in similarly treated wild-type mice. In the knockout mice on the high-salt diet there was an impairment of urinary sodium excretion and an increase in body weight, but no elevation of plasma renin or serum aldosterone levels. When the knockout mice on the high-salt diet were treated with amiloride, an epithelial sodium channel blocker that inhibits renal sodium reabsorption, the impaired urinary sodium excretion and increased body weight were normalized. Amiloride treatment also reduced high blood pressure caused by the high-salt diet in these mice. Thus, the lack of corin in mice impairs their adaptive renal response to high dietary salt, suggesting that corin deficiency may represent an important mechanism underlying salt-sensitive hypertension.

Show MeSH
Related in: MedlinePlus