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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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Levels of plasma renin and serum aldosterone in WT and Cor−/− miceMice were on 0.3% or 4% NaCl diets. Plasma renin (a) and serum aldosterone (b) levels were measured, as described in Methods. n=7–8 per group. P values by two-way ANOVA were shown. n.s., not statistically significant.
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Figure 4: Levels of plasma renin and serum aldosterone in WT and Cor−/− miceMice were on 0.3% or 4% NaCl diets. Plasma renin (a) and serum aldosterone (b) levels were measured, as described in Methods. n=7–8 per group. P values by two-way ANOVA were shown. n.s., not statistically significant.

Mentions: To examine if an enhanced renin-angiotensin-aldosterone system (RAAS) may be responsible for hypertension and sodium-water retention in Cor−/− mice, we measured plasma renin concentration (PRC) and serum aldosterone. Similar plasma renin levels were found in WT and Cor−/− mice on the normal salt diet (Figure 4a). On the high salt diet, both groups had significantly lower PRC, indicating that renin levels were suppressed. There was no significant difference in PRC between the two groups (Figure 4a). Serum aldosterone levels were found to be lower in Cor−/− than that in WT mice on both the normal and high salt diets (Figure 4b). The results indicated that an enhanced RAAS was unlikely to be present in Cor−/− mice.


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)

Levels of plasma renin and serum aldosterone in WT and Cor−/− miceMice were on 0.3% or 4% NaCl diets. Plasma renin (a) and serum aldosterone (b) levels were measured, as described in Methods. n=7–8 per group. P values 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 4: Levels of plasma renin and serum aldosterone in WT and Cor−/− miceMice were on 0.3% or 4% NaCl diets. Plasma renin (a) and serum aldosterone (b) levels were measured, as described in Methods. n=7–8 per group. P values by two-way ANOVA were shown. n.s., not statistically significant.
Mentions: To examine if an enhanced renin-angiotensin-aldosterone system (RAAS) may be responsible for hypertension and sodium-water retention in Cor−/− mice, we measured plasma renin concentration (PRC) and serum aldosterone. Similar plasma renin levels were found in WT and Cor−/− mice on the normal salt diet (Figure 4a). On the high salt diet, both groups had significantly lower PRC, indicating that renin levels were suppressed. There was no significant difference in PRC between the two groups (Figure 4a). Serum aldosterone levels were found to be lower in Cor−/− than that in WT mice on both the normal and high salt diets (Figure 4b). The results indicated that an enhanced RAAS was unlikely to be present in Cor−/− mice.

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