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High-salt intake accelerates functional and histological renal damage associated with renal tissue overexpression of (pro)renin receptors and AT1 receptors in spontaneously hypertensive rats

Abstract

Objective

This study aimed to investigate the effect of combination of high-salt intake and hypertension on renal functional and histological damage, associated with renal (pro)renin receptor [(P)RR] and AT1 receptor in rats.

Methods

Wistar Kyoto rats (WKYs) and spontaneously hypertensive rats (SHRs) received regular rat chow (normal-salt diet 0.9%) or high-salt rat chow (high-salt diet 8.9%) for 6 weeks from 6 to 12 weeks of age. Systolic blood pressure, serum creatinine and blood urea nitrogen (BUN) were measured. Histological analysis of the kidney was performed. Western blot analysis was performed on the expressions of (P)RR, angiotensinogen and AT1 receptor in the kidney.

Results

High-salt intake significantly increased systolic blood pressure in WKYs and especially in SHRs. High-salt intake significantly increased serum creatinine and BUN, and accelerated renal tubulointerstitial fibrosis and glomerular sclerosis in SHRs. High-salt intake significantly enhanced the renal tissue expressions of (P)RR, angiotensinogen and AT1 receptor in SHRs.

Conclusion

High-salt intake accelerates functional and histological renal damage associated with renal tissue overexpression of (P)RR and AT1 receptors in SHRs.

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Acknowledgements

The authors thank Miss Yoshie Arai for technical assistance.

Funding

This work was supported by a grant from the Gifu University Graduate School of Medicine (to S. Minatoguchi).

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Correspondence to Shinya Minatoguchi.

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All the authors have declared no conflict of interest.

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All procedures performed in studies involving animals were in accordance with the ethical standards of the institution or practice at which the studies were conducted (IRB approval number 24-9).

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Hayakawa, Y., Komaki, H., Minatoguchi, S. et al. High-salt intake accelerates functional and histological renal damage associated with renal tissue overexpression of (pro)renin receptors and AT1 receptors in spontaneously hypertensive rats. Clin Exp Nephrol 24, 582–589 (2020). https://doi.org/10.1007/s10157-020-01888-7

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Keywords

  • Salt
  • Hypertension
  • (pro)renin receptor
  • Angiotensin II AT1 receptor
  • Renal damage