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Background  Mineralocorticoid receptor ( MR ) has pathological roles in various cell types, including renal tubule cells, myocytes, and smooth muscle cells; however, the role of  MR  in intestinal epithelial cells ( IECs ) has not been sufficiently evaluated. The intestine is the sensing organ of ingested sodium; accordingly, intestinal  MR  is expected to have essential roles in blood pressure (BP) regulation.    Methods and Results  We generated  IEC ‐specific  MR  knockout ( IEC ‐ MR ‐ KO ) mice. With a standard diet, fecal sodium excretion was 1.5‐fold higher in  IEC ‐ MR ‐ KO  mice, with markedly decreased colonic expression of β‐ and γ‐epithelial sodium channel, than in control mice. Urinary sodium excretion in  IEC ‐ MR ‐ KO  mice decreased by 30%, maintaining sodium balance; however, a low‐salt diet caused significant reductions in body weight and BP in  IEC ‐ MR ‐ KO  mice, and plasma aldosterone exhibited a compensatory increase. With a high‐salt diet, intestinal sodium absorption markedly increased to similar levels in both genotypes, without an elevation in BP. Deoxycorticosterone/salt treatment elevated BP and increased intestinal sodium absorption in both genotypes. Notably, the increase in BP was significantly smaller in  IEC ‐ MR ‐ KO  mice than in control mice. The addition of the  MR  antagonist spironolactone to deoxycorticosterone/salt treatment eliminated the differences in BP and intestinal sodium absorption between genotypes.    Conclusions  Intestinal  MR  regulates intestinal sodium absorption in the colon and contributes to BP regulation. These regulatory effects are associated with variation in epithelial sodium channel expression. These findings suggest that intestinal  MR  is a new target for studying the molecular mechanism of hypertension and cardiovascular diseases.

Intestinal Mineralocorticoid Receptor Contributes to Epithelial Sodium Channel–Mediated Intestinal Sodium Absorption and Blood Pressure Regulation