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(Hypertension. 2008;52:618.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

Gene Targeting and Heme Oxygenase-1 Expression in Prevention of Hypertension Induced by Angiotensin II

Nader G. Abraham

From the Department of Pharmacology and Medicine, New York Medical College, Valhalla.

Correspondence to Nader G. Abraham, Department of Pharmacology and Medicine, New York Medical College, Basic Science Building, Valhalla, NY 10595. E-mail nader_abraham@nymc.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The report by Vera et al¹ that appears in this issue demonstrates that the kidney-specific induction of heme oxygenase (HO)-1 prevents angiotensin (Ang) II hypertension in CL57BL/6J mice. Kidney-specific induction of HO-1 was achieved by implanting intrarenal medullary interstitial catheters in the left kidney of uninephrectomized mice. Infusion of cobalt protoporphyrin, a known inducer of HO-1, produced a significant induction of HO-1 protein levels and increased HO activity largely in the renal medulla. Ang II–dependent hypertension was examined by measuring mean arterial pressure and was found to be attenuated in cobalt protoporphyrin–treated animals. The levels of heme, the substrate of HO, and superoxide were increased in Ang II–treated animal. These increases were blocked in cobalt protoporphyrin–treated animals. The authors conclude that the specific induction of renal HO-1 is responsible for the prevention of Ang II–dependent hypertension and the lowering of blood pressure in this animal model of hypertension.

This article raises important findings related to gene targeting in renal injury and HO-1. As shown previously, the degradation of heme is regarded as pivotal in cellular defense for 2 reasons. First, the pro-oxidant heme is removed and, second, increased production of bilirubin/biliverdin and CO, heme degradation products, is now considered beneficial to cellular cytoprotection. Iron, the third heme degradation product, which can stimulate free radical formation, is immediately bound by ferritin. Thus, CO and bilirubin are central to the defense mechanisms that occur in times of stress, a result of elevated levels of HO-1 protein and HO activity. The HO-1/HO-2 system . . . [Full Text of this Article]

Related Article:

Kidney-Specific Induction of Heme Oxygenase-1 Prevents Angiotensin II Hypertension

Trinity Vera, Silvia Kelsen, and David E. Stec
Hypertension 2008 52: 660-665. [Abstract] [Full Text] [PDF]

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				R. S. Danziger Use of Protoporphyrins to Evaluate Heme Oxygenase Problematical Hypertension, February 1, 2009; 53(2): e15 - e15. [Full Text] [PDF]