High perfusion pressure accelerates renal injury in salt-sensitive hypertension

Takefumi Mori, Aaron Polichnowski, Padden Glocka, Mary Kaldunski, Yusuke Ohsaki, Mingyu Liang, Allen W. Cowley

Research output: Contribution to journalArticle

69 Citations (Scopus)

Abstract

Renal injury in the Dahl salt-sensitive rat mimics human salt-sensitive forms of hypertension that are particularly prevalent in black individuals, but the mechanisms that lead to the development of this injury are incompletely understood. We studied the impact of renal perfusion pressure (RPP) on the development of renal injury in this model. During the development of salt-induced hypertension over 2 wk, the RPP to the left kidney was maintained at control levels (125 ± 2 mmHg) by continuous servocontrol inflation of an aortic balloon implanted between the renal arteries; during the same period, the RPP to the right kidney rose to 164 ± 8 mmHg. After 2 wk of a 4% salt diet, DNA microarray and real-time PCR identified genes related to fibrosis and epithelial-to-mesenchymal transition in the kidneys exposed to hypertension. The increased RPP to the right kidney accounted for differences in renal injury between the two kidneys, measured by percentage of injured cortical and juxtamedullary glomeruli, quantified proteinaceous casts, number of ED-1-positive cells per glomerular tuft area, and interstitial fibrosis. Interlobular arteriolar injury was not increased in the kidney exposed to elevated pressure but was reduced in the control kidney. We conclude that elevations of RPP contribute significantly to the fibrosis and epithelial-to-mesenchymal transition found in the early phases of hypertension in the salt-sensitive rat.

Original languageEnglish
Pages (from-to)1472-1482
Number of pages11
JournalJournal of the American Society of Nephrology
Volume19
Issue number8
DOIs
Publication statusPublished - 2008 Aug 1

ASJC Scopus subject areas

  • Nephrology

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