ArticleAmerican journal of physiology. Renal physiology2011
Inhibition of heme oxygenase augments tubular sodium reabsorption.
Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- The roles of heme oxygenase-1 in renal disease.Frontiers in nephrology · 2023Review
- (Pro)renin receptor contributes to regulation of renal epithelial sodium channel.Journal of hypertension · 2016Article
- An emerging role for gasotransmitters in the control of breathing and ionic regulation in fish.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2016Review
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- Heme induction with delta-aminolevulinic Acid stimulates an increase in water and electrolyte excretion.International journal of hypertension · 2012Article
- Renal heme oxygenase-1 induction with hemin augments renal hemodynamics, renal autoregulation, and excretory function.International journal of hypertension · 2012Article
- Gasotransmitters: novel regulators of epithelial na(+) transport?Frontiers in physiology · 2012Article
- Bilirubin, renal hemodynamics, and blood pressure.Frontiers in pharmacology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Heme oxygenase (HO) catalyzes the degradation of heme to form iron, biliverdin, and carbon monoxide (CO). The vascular actions of CO include direct vasodilation of vascular smooth muscle and indirect vasoconstriction through inhibition of nitric oxide synthase (NOS). This study was performed to examine the effects in the kidney of inhibition of heme oxygenase alone or combined with NOS inhibition. Chromium mesoporphyrin (CrMP; 45 μmol/kg ip), a photostable HO inhibitor, was given to control rats and N(G)-nitro-l-arginine methyl ester (l-NAME)-treated hypertensive rats (50 mg·kg⁻¹·day⁻¹), 12 h, 4 days). In control animals, CrMP decreased CO levels, renal HO-1 levels, urine volume, and sodium excretion, but had no effect on arterial pressure, renal blood flow (RBF), plasma renin activity (PRA), or glomerular filtration rate (GFR). In l-NAME-treated hypertensive rats, CrMP decreased endogenous CO and renal HO-1 levels and had no effect on arterial pressure, RBF, or GFR but decreased sodium and water excretion in a similar manner to control animals. An increase in PRA was observed in untreated rats but not in l-NAME-infused rats, indicating that this effect is associated with an absent NO system. The results suggest that inhibition of HO promotes water and sodium excretion by a direct tubular action that is independent of renal hemodynamics or the NO system.
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Registered trials
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