Fig. 6.

Effect of renal damage on renin expression and effect of RAS inhibition on kidney regeneration. To test responses of ren transcription to renal injury and regeneration, mRNA expression was tested in whole kidney. The role for RAS during regeneration was tested using captopril RAS inhibition from 24 h postinjection. Renal damage was induced by 65 mg/kg intraperitoneal (ip) gentamicin (Gen) injection and analyzed 2 days postinjection (dpi). Whole kidneys were analyzed both with and without 0.5 mM waterborne captopril (Capt) during kidney regeneration at 8 dpi. A: the decrease of the proximal tubular marker, solute carrier slc20a1a, confirms damage of the proximal tubule at both 2 and 8 dpi. B: kidney damage is also confirmed by the upregulation of kidney injury molecule (kim1) at 2 and 8 dpi. C and D: the slight increase of both Wilm's tumor homologs is not significant at 8 dpi. Wilm's tumor 1b is upregulated in regenerating kidneys subject to captopril treatment. E: the nephron progenitor marker LIM homeobox 1a (lhx1a) is upregulated 8 days postinjection confirming a regenerative response. Expression of lhx1a is not affected by captopril treatment. F: renin mRNA is upregulated with the renal injury at 2 dpi. Expression of ren subsequently decreases to control levels after the renal tissue progresses from an injury phase to regeneration at 8 dpi. As occurs under normal conditions, renin expression is increased by captopril in regenerating kidneys. P value summary: ns, P ≥ 0.123; *P ≤ 0.033; **P ≤ 0.002; and ***P ≤ 0.001.