Collecting duct-specific knockout of the endothelin B receptor causes hypertension and sodium retention.

Explorer Combined knockout of collecting duct endothelin A and B receptors causes hypertension and sodium retention

Combined knockout of collecting duct endothelin A and B receptors causes hypertension and sodium retention.

The collecting duct (CD) endothelin (ET) system regulates blood pressure (BP) and Na excretion. CD-specific knockout (KO) of ET-1 causes hypertension, CD-specific KO of the ETA receptor does not alter BP, while CD-specific KO of the ETB receptor increases BP to a lesser extent than CD ET-1 KO. These findings suggest a paracrine role for CD-derived ET-1; however, they do not exclude compensation...

Collecting duct-specific endothelin B receptor knockout increases ENaC activity.

Collecting duct (CD)-derived endothelin-1 (ET-1) acting via endothelin B (ETB) receptors promotes Na(+) excretion. Compromise of ET-1 signaling or ETB receptors in the CD cause sodium retention and increase blood pressure. Activity of the epithelial Na(+) channel (ENaC) is limiting for Na(+) reabsorption in the CD. To test for ETB receptor regulation of ENaC, we combined patch-clamp electrophys...

Physiological actions of renal collecting duct endothelin.

THE CONTRIBUTION OF ENDOTHELIN to regulation of renal function under normal physiological conditions is unclear. Many cells in the kidney produce endothelin (9). Endothelin has been reported to have effects that both promote (2, 3, 5–7, 12–14, 16, 18) and reduce (2, 8, 13, 15) urinary sodium excretion and urinary volume. This may be due to the fact that endothelin exerts its effects via two rec...

Collecting duct-specific knockout of endothelin-1 causes hypertension and sodium retention.

In vitro studies suggest that collecting duct-derived (CD-derived) endothelin-1 (ET-1) can regulate renal Na reabsorption; however, the physiologic role of CD-derived ET-1 is unknown. Consequently, the physiologic effect of selective disruption of the ET-1 gene in the CD of mice was determined. Mice heterozygous for aquaporin2 promoter Cre recombinase and homozygous for loxP-flanked exon 2 of t...