Why the study?
Exchange proteins directly activated by cAMP (Epacs) are abundantly expressed in renal tubules, but the role of Epac1 and Epac2 in renal sodium handling remained to be examined.
Does genetic deletion or pharmacological inhibition of Epac1 and Epac2 impair renal sodium conservation and ENaC activity in mice?
Population
Epac1-/-, Epac2-/-, and Epac WT mice
Comparison
Epac1-/-, Epac2-/-, or pharmacologically blocked mice vs WT mice on Na+-deficient or regular diets
Design
Preclinical animal study using genetic, pharmacological, balance, electrophysiological, and biochemical approaches
Authors
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Epac deletion impairs sodium conservation in salt-restricted mice; hypothesis-generating for Epac inhibition in ENaC-driven hypertension.
Does genetic deletion or pharmacological inhibition of Epac1 and Epac2 impair renal sodium conservation and ENaC activity in mice?
Epac1 and Epac2 have nonredundant roles in stimulating ENaC activity during dietary salt restriction, suggesting Epac inhibition could be a potential therapeutic target for hypertensive states associated with ENaC overactivation.
Tomilin et al. (2021) studied this question.
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