This Article Full Text Full Text (PDF) All Versions of this Article: 49/1/23    most recent 01.HYP.0000250089.99513.f6v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Pallone, T. L. Search for Related Content PubMed PubMed Citation Articles by Pallone, T. L. Related Collections Other hypertension Hypertension - basic studies Ion channels/membrane transport Other etiology Endothelium/vascular type/nitric oxide Other Vascular biology Related Article

(Hypertension. 2007;49:23.)
© 2007 American Heart Association, Inc.

Editorial Commentaries

Control of Renal Na⁺ Excretion by Heme Oxygenase

Thomas L. Pallone

From the Division of Nephrology, Departments of Medicine and Physiology, 22 S. Greene St, N3W143, University of Maryland at Baltimore.

Correspondence to Thomas L. Pallone, MD, Division of Nephrology, N3W143, 22 S. Greene St, UMMS, Baltimore, MD 21201. E-mail tpallone@medicine.umaryland.edu

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

In the current issue of Hypertension, Li et al provide evidence that supports acute and chronic roles for renal medullary heme oxygenase (HO) in the regulation of salt and water excretion by the kidney.¹ Their findings may be summarized as follows: HO activity and expression rises with medullary axis; inner medulla >outer medulla >cortex. Acute elevation of renal perfusion pressure (RPP) induces a rise in the medullary tissue carbon monoxide (CO) and NO concentrations accompanied by natriuresis. Chromium mesoporphyrin (CrMP) inhibits the HO activity of medullary homogenates and, when infused into the renal interstitium, reduces both basal- and RPP-stimulated CO, NO levels, and salt and water excretion. Li and colleagues carried their investigation an important step further by examining chronic interstitial infusion of CrMP in rats maintained on either a 1% or 8% NaCl diet. Those on a 1% NaCl diet experienced a transient, 1-week elevation of mean arterial pressure of 5 to 10 mm Hg. By comparison, on an 8% NaCl diet, CrMP induced a sustained and impressive rise of 25 to 30 mm Hg. Finally, expression and activity of inducible HO-1 but not HO-2 was increased by the high salt diet.

The effectiveness of basal HO blockade shows a tonic effect of the products of heme degradation on epithelial Na⁺ reabsorption. Moreover, HO inhibition by CrMP blunts the diuresis and natriuresis associated with an acute increase in RPP; it blocks "pressure natriuresis" (Figure). These fundamental findings point to the importance of HO in the regulation . . . [Full Text of this Article]

Related Article:

Role of Renal Medullary Heme Oxygenase in the Regulation of Pressure Natriuresis and Arterial Blood Pressure

Ningjun Li, Fan Yi, Elisabete A. dos Santos, Dustin K. Donley, and Pin-Lan Li
Hypertension 2007 49: 148-154. [Abstract] [Full Text] [PDF]