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The Modulatory Role of Heme Oxygenase on Subpressor Angiotensin II-Induced Hypertension and Renal Injury

Authors :
Kiran Chandrashekar
Arnaldo Lopez-Ruiz
Ramiro Juncos
Karl Nath
David E. Stec
Trinity Vera
Ruisheng Liu
Luis A. Juncos
Source :
International Journal of Hypertension, Vol 2012 (2012)
Publication Year :
2012
Publisher :
Hindawi Limited, 2012.

Abstract

Angiotensin II (AngII) causes hypertension (HTN) and promotes renal injury while simultaneously inducing reno-protective enzymes like heme oxygenase-1 (HO-1). We examined the modulatory role of HO on sub-pressor angiotensin II (SP-AngII) induced renal inflammation and injury. We first tested whether the SP-AngII-induced renal dysfunction, inflammation and injury are exacerbated by either preventing (chronic HO-1 inhibition) or reversing (late HO-1 inhibition) SP-AngII-induced HO (using tin protoporphyrin; SnPP). We next examined whether additional chronic or late induction of SP-AngII-induced HO (using cobalt protoporphyrin; CoPP), prevents or ameliorates renal damage. We found that neither chronic nor late SnPP altered blood pressure. Chronic SnPP worsened SP-AngII-induced renal dysfunction, inflammation, injury and fibrosis, whereas late SnPP worsened renal dysfunction but not inflammation. Chronic CoPP prevented HTN, renal dysfunction, inflammation and fibrosis, but surprisingly, not the NGAL levels (renal injury marker). Late CoPP did not significantly alter SP-AngII-induced HTN, renal inflammation or injury, but improved renal function. Thus, we conclude (a) endogenous HO may be an essential determining factor in SP-AngII induced renal inflammation, injury and fibrosis, (b) part of HO’s renoprotection may be independent of blood pressure changes; and (c) further induction of HO-1 protects against renal injury, suggesting a possible therapeutic target.

Details

Language :
English
ISSN :
20900384 and 20900392
Volume :
2012
Database :
Directory of Open Access Journals
Journal :
International Journal of Hypertension
Publication Type :
Academic Journal
Accession number :
edsdoj.0025460cdfc4486b45dda9d2f2b6004
Document Type :
article
Full Text :
https://doi.org/10.1155/2012/392890