Collecting Duct Collects ET 1 Data
Donald Kohan and colleagues, from the University of Utah Health Sciences Center, have now created a mouse model in which ET-1 is selectively disrupted in the collecting duct (CD) and investigated its physiological importance.
These mice, when fed a normal Na diet, were hypertensive, but their body weight, Na excretion, urinary aldosterone excretion and plasma renin activity were similar to those in wild-type mice. When the mice were given a high-Na diet, hypertension worsened, but they additionally had excessive weight gain and reduced Na excretion, which indicates that ET-1 affects salt retention under Na-loading conditions.
Treatment of normal- or high-Na-diet mice with the natriuretic agents amiloride or furosemide reduced blood pressure and alleviated Na retention, which suggests that CD-derived ET-1 regulates Na reabsorption through inhibition of tubule Na reabsorption. These data define an important physiological role for CD-derived ET-1 in regulating systemic blood pressure and renal Na excretion.
TITLE: Collecting duct-specific knockout of endothelin-1 causes hypertension and sodium retention
AUTHOR CONTACT:
Donald E. Kohan University of Utah Health Sciences Center, Salt Lake City, UT 84132, USA
Phone: (801) 581-6709; Fax: (801) 581-4343; E-mail: donald.kohan@hsc.utah.edu
View the PDF of this article at: https://www.the-jci.org/press/21064.pdf
Contact: Laurie Goodman
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
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