Water Deprivation Increases (Pro)renin Receptor Levels in the Kidney and Decreases Plasma Concentrations of Soluble (Pro)renin Receptor

  • Tamura Yuma
    Department of Internal Medicine and Rehabilitation Science, Tohoku University Graduate School of Medicine
  • Mori Nobuyoshi
    Department of Internal Medicine and Rehabilitation Science, Tohoku University Graduate School of Medicine
  • Xu Bin
    Department of Internal Medicine and Rehabilitation Science, Tohoku University Graduate School of Medicine
  • Nakamura Takahiro
    Department of Internal Medicine and Rehabilitation Science, Tohoku University Graduate School of Medicine
  • Yamakoshi Seiko
    Department of Internal Medicine and Rehabilitation Science, Tohoku University Graduate School of Medicine
  • Hirose Takuo
    Division of Nephrology, Endocrinology, and Vascular Medicine, Department of Medicine, Tohoku University Graduate School of Medicine
  • Ito Osamu
    Department of Internal Medicine and Rehabilitation Science, Tohoku University Graduate School of Medicine
  • Totsune Kazuhito
    Department of Social Welfare, Faculty of Synthetic Welfare, Tohoku Fukushi University
  • Takahashi Kazuhiro
    Department of Endocrinology and Applied Medical Science, Tohoku University Graduate School of Medicine
  • Kohzuki Masahiro
    Department of Internal Medicine and Rehabilitation Science, Tohoku University Graduate School of Medicine

Abstract

Water deprivation activates the renin-angiotensin system. We have hypothesized that the renal expression of (pro)renin receptor ((P)RR), a specific receptor for renin and prorenin, could be changed under dehydration. Moreover, plasma levels of soluble (P)RR (s(P)RR) comprising of the extracellular domain of (P)RR may reflect the renal (P)RR expression. In the present study, we therefore aimed to clarify changes of plasma s(P)RR concentrations and kidney tissue (P)RR levels using rats with dehydration. Male Wister-Kyoto rats were divided into two groups; dehydrated (DH) rats deprived of water for 72 hours with free access to food, and control rats. Plasma s(P)RR concentrations measured by enzyme-linked immunosorbent assay were significantly lower in DH rats (6.94 ± 2.08 ng/mL, mean ± SD, n = 5) than in control (12.54 ± 2.00 ng/mL, n = 5) (p < 0.05). Western blot analysis confirmed lower expression levels of s(P)RR in plasma in DH rats than in control. By contrast, western blot analysis showed higher levels of full-length (P)RR and lower levels of furin (an enzyme responsible for generation of s(P)RR from full-length (P)RR) in the kidney tissues obtained from DH rats compared to control. There was no significant difference in the renal (P)RR mRNA levels between DH rats and control. These findings suggest that water deprivation may elevate the renal full-length (P)RR levels via reducing the expression of furin. Increased full-length (P)RR may contribute to the up-regulation of the renal renin-angiotensin system and the production of concentrated urine under dehydration.

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