Within the kidney the expression of the aldo-keto reductase Akr1b7 is restricted to renin secreting cells (Brunskill et al., J Am Soc. Nephrol. 2011). Whilst the expression of renin appears not to be crucial for the expression of Akr1b7, it is unknown if Akr1b7 function is relevant for renin synthesis and secretion.

Therefore our study aimed to assess the impact of Akr1b7 on renin synthesis and secretion by characterizing the renin system in Akr1b7 deficient mice.

We could confirm coimmunolocalization of Akr1b7 with renin in wildtype kidneys. Renin producing cells in Akr1b7-/- kidneys displayed normal numbers and localization. Renin mRNA abundance in Akr1b7-/- mice was normal, as was plasma renin activity. Renin secretion in Akr1b7-/- kidneys was stimulated by isoproterenol as in wildtype kidneys and also pressure dependent renin secretion was not different between the two genotypes. In line, also blood pressure was normal in Akr1b7-/- mice.

As a summary, or findings confirm the coexpression of Akr1b7 and of renin in the kidney. Our findings further indicate that Akr1b7 is not required for normal regulation of renin gene expression and renin secretion. Along with the previous report which states that renin expression is not essential for Akr1b7 expression, our findings suggest that the expression of both genes is cell type specific, but is without functional interdependency.