Collecting duct–specific knockout of endothelin-1 causes hypertension and sodium retention
Removing endothelin-1 in kidney water-filtering cells may cause high blood pressure and salt buildup
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Abstract
Mice lacking collecting duct-derived endothelin-1 (ET-1) exhibited significant hypertension on normal and high sodium diets.
- Disruption of the ET-1 gene in the collecting duct resulted in no detectable CD ET-1 mRNA and reduced urinary ET-1 excretion.
- Hypertension was observed in CD ET-1 KO mice on both normal and high sodium diets, suggesting a role for CD-derived ET-1 in blood pressure regulation.
- Despite changes in blood pressure, body weight, sodium excretion, urinary aldosterone excretion, and plasma renin activity remained unchanged in CD ET-1 KO mice on a normal sodium diet.
- On a high sodium diet, CD ET-1 KO mice experienced worsened hypertension, reduced urinary sodium excretion, and excessive weight gain.
- Blood pressure was lowered in CD ET-1 KO mice treated with amiloride or furosemide, indicating potential therapeutic avenues for managing hypertension in these mice.
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