Angiotensin II upregulates CYP4A isoform expression in the rat kidney through angiotensin II type 1 receptor

Rong Rong, Gaizun Hu, Wanting Wang, Yoshikazu Muroya, Takahiro Miura, Yoshiko Ogawa, Masahiro Kohzuki, Osamu Ito

Research output: Contribution to journalArticlepeer-review

Abstract

Angiotensin II (AngII) stimulates the renal production and release of 20-hydroxyeicosatetraenoic acids (20-HETE), which is a major metabolite of arachidonic acid catalyzed by CYP4A isoforms. However, the effects of AngII on CYP4A isoform expression in the kidney and its mechanism remains unclear. To clarify the regulation of CYP4A isoform expression by AngII, we examined the chronic effects of AngII and AngII type 1 receptor (AT1-R) blockade on CYP4A isoform expression. Sprague-Dawley rats were infused with vehicle or AngII for 1 week, and the AngII-infused rats were also treated with or without the AT1-R blocker, candesartan. AngII increased CYP4A isoform protein expression in the renal cortex (CO) and outer medulla (OM) in a dose-dependent manner, and candesartan inhibited the AngII-increased CYP4A expression in a dose-dependent manner. AngII increased the CYP4A isoform mRNA expression in the CO and OM, and candesartan inhibited AngII-increased CYP4A isoform mRNA expression. These results indicated that AngII chronically increased the CYP4A isoform expression in the rat kidney. The AngII-induced CYP4A isoform expression was mediated by AT1-R.

Original languageEnglish
Pages (from-to)80-86
Number of pages7
JournalProstaglandins and Other Lipid Mediators
Volume139
DOIs
Publication statusPublished - 2018 Nov

Keywords

  • 20-Hydroxyeicosatetraenoic acids
  • Angiotensin II type 1 receptor
  • Cytochrome P-450 4A
  • Hypertension
  • Kidney

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Pharmacology
  • Cell Biology

Fingerprint

Dive into the research topics of 'Angiotensin II upregulates CYP4A isoform expression in the rat kidney through angiotensin II type 1 receptor'. Together they form a unique fingerprint.

Cite this