Role of natriuretic peptide receptor type C in Dahl salt-sensitive hypertensive rats

Miki Nagase, Katsuyuki Ando, Takeshi Katafuchi, Akira Kato, Shigehisa Hirose, Toshiro Fujita

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


The natriuretic peptide system is suggested to be involved in the pathogenesis of salt-sensitive hypertension; a recent report indicated that disruption of the atrial natriuretic peptide precursor gene caused salt- sensitive hypertension. However, natriuretic peptide receptor (NPR)-A knockout mice did not show enhanced salt sensitivity of blood pressure. The aim of the present study was to investigate the role of NPR-C, the other receptor for atrial natriuretic peptide, in increased salt sensitivity of blood pressure. Dahl salt-sensitive (DS) and salt-resistant (DR) rats were placed on a 0.3% or 8% NaCl diet for 4 weeks. Blood pressure was elevated by salt loading only in DS rats. RNase protection assay demonstrated that NPR-C transcript level in the kidney was reduced by chronic salt loading in both DR and DS rats, whereas expression of NPR-A and NPR-B was not altered. The reduction of NPR-C mRNA in response to salt loading was enhanced in DS compared with DR rats. In situ hybridization indicated that the salt-induced NPR-C change was attributed mainly to suppressed expression of NPR-C in the podocytes. NPR-C gene expression was regulated by salt loading in a tissue- specific manner; the marked decrease in NPR-C mRNA by salt loading was seen only in the kidney. These data suggest that the exaggerated salt-induced reduction of NPR-C in the kidney of DS rats may play an important role in the pathogenesis of salt hypertension in this animal, possibly related to impaired renal sodium excretion.

Original languageEnglish (US)
Pages (from-to)177-183
Number of pages7
Issue number2
StatePublished - Aug 1997


  • Atrial natriuretic factor
  • Dahl salt-sensitive
  • Gene expression
  • In situ hybridization
  • Receptors
  • Sodium
  • rats

ASJC Scopus subject areas

  • Internal Medicine


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