Effect of lisinopril on deposition of iron in renal tissue in Tsukuba hypertensive mice carrying human renin‐angiotensin system genes

SUMMARY: Tsukuba hypertensive mice (THM) are transgenic mice that carry both human renin and angiotensinogen genes and overexpress the human renin-angiotensin system (RAS). In the present study, the effect of lisinopril on deposition of macromolecular iron in renal tissue in THM was evaluated. Twelve-week-old male THM were divided into the following groups: lisinopril dosage group (ACEI group), hydralazine dosage group (hydralazine group), and a no-drug group (control group). Age-matched male C57BL/6 mice (wild group) were used as normal controls. Each mouse was treated with a drug for 8 weeks. All mice were euthanised at 20 weeks of age, and their kidneys were fixed and stained with Berlin-blue. Systolic blood pressure was significantly higher in the control group than in the wild group, and it decreased significantly to similar levels in the ACEI group and the hydralazine group. Iron deposition was observed in proximal renal tubules in the control group and the hydralazine group, but iron deposition was not observed in the ACEI group or the wild group. The results of the study suggest that the RAS plays an important role in the deposition of iron in the proximal renal tubules in THM, and that lisinopril prevents this deposition.