Removing both types of endothelin receptors in the kidney's collecting duct leads to high blood pressure and salt buildup

CD-specific knockout of both ETA and ETB receptors leads to increased blood pressure and reduced sodium excretion.

• Knockout of ET-1 in the collecting duct causes hypertension, while knockout of the ETA receptor does not alter blood pressure.
• Knockout of the ETB receptor increases blood pressure, but to a lesser extent than ET-1 knockout.
• Mice with knockout of both ETA and ETB receptors excreted less urinary sodium during both acute and chronic sodium loading.
• Despite similar urinary aldosterone and plasma renin levels, CD ETA/B knockout mice exhibited salt-sensitive hypertension.
• Combined deficiency of CD ETA and ETB receptors results in a greater increase in blood pressure than the loss of either receptor alone.

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