ArticleAmerican journal of physiology. Renal physiology2008
Heme oxygenase metabolites inhibit tubuloglomerular feedback (TGF).
Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Carbon Monoxide Signaling: Examining Its Engagement with Various Molecular Targets in the Context of Binding Affinity, Concentration, and Biologic Response.Pharmacological reviews · 2022Review
- Carbon monoxide: An emerging therapy for acute kidney injury.Medicinal research reviews · 2020Review
- Heme Oxygenases in Cardiovascular Health and Disease.Physiological reviews · 2016Review
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- Heme oxygenase-1 and acute kidney injury.Current opinion in nephrology and hypertension · 2014Review
- Mechanism of inhibition of tubuloglomerular feedback by CO and cGMP.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Mechanisms of carbon monoxide attenuation of tubuloglomerular feedback.Hypertension (Dallas, Tex. : 1979) · 2012Article
- Role of carbon monoxide in kidney function: is a little carbon monoxide good for the kidney?Current pharmaceutical biotechnology · 2012Review
- Aberrant tubuloglomerular feedback and HIF-1α confer resistance to ischemia after subtotal nephrectomy.Journal of the American Society of Nephrology : JASN · 2012Article
- Bilirubin, renal hemodynamics, and blood pressure.Frontiers in pharmacology · 2012Article
- Heme oxygenase metabolites inhibit tubuloglomerular feedback in vivo.American journal of physiology. Heart and circulatory physiology · 2011Article
- The therapeutic potential of carbon monoxide.Nature reviews. Drug discovery · 2010Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Tubuloglomerular feedback (TGF) is the mechanism by which the macula densa (MD) senses increases in luminal NaCl concentration and sends a signal to constrict the afferent arteriole (Af-Art). The kidney expresses constitutively heme oxygenase-2 (HO-2) and low levels of HO-1. HOs release carbon monoxide (CO), biliverdin, and free iron. We hypothesized that renal HOs inhibit TGF via release of CO and biliverdin. Rabbit Af-Arts and attached MD were simultaneously microperfused in vitro. The TGF response was determined by measuring Af-Art diameter before and after increasing NaCl in the MD perfusate. When HO activity was inhibited by adding stannous mesoporphyrin (SnMP) to the MD perfusate, the TGF response increased from 2.1+/-0.2 to 4.1+/-0.4 microm (P=0.003, control vs. SnMP, n=7). When a CO-releasing molecule, (CORM-3; 50 microM), was added to the MD perfusate, the TGF response decreased by 41%, from 3.6+/-0.3 to 2.1+/-0.2 microm (P<0.001, control vs. CORM-3, n=12). When CORM-3 at 100 microM was added to the perfusate, it completely blocked the TGF response, from 4.2+/-0.4 to -0.2+/-0.3 microm (P<0.001, control vs. CORM-3, n=6). When biliverdin was added to the perfusate, the TGF response decreased by 79%, from 3.4+/-0.3 to 0.7+/-0.4 microm (P=0.001, control vs. biliverdin, n=6). The effects of SnMP and CORM-3 were not blocked by inhibition of nitric oxide synthase. We concluded that renal HO inhibits TGF probably via release of CO and biliverdin. HO regulation of TGF is a novel mechanism that could lead to a better understanding of the control of renal microcirculation and function.
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