ArticleAmerican journal of physiology. Renal physiology2016
Impact of nitric-oxide-mediated vasodilation and oxidative stress on renal medullary oxygenation: a modeling study.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 33 citations in OpenAlex.
- Sex and circadian regulation of metabolic demands in the rat kidney: A modeling analysis.PloS one · 2024Article
- Sex differences in the renin-angiotensin-aldosterone system and its roles in hypertension, cardiovascular, and kidney diseases.Frontiers in cardiovascular medicine · 2023Review
- Effect of pregnancy and hypertension on kidney function in female rats: Modeling and functional implications.PloS one · 2023Article
- Sex differences in circadian regulation of kidney function of the mouse.American journal of physiology. Renal physiology · 2022Article
- Renal blood flow and oxygenation.Pflugers Archiv : European journal of physiology · 2022Review
- Sex-Specific Computational Models of Kidney Function in Patients With Diabetes.Frontiers in physiology · 2022Article
- Sex differences in solute and water handling in the human kidney: Modeling and functional implications.iScience · 2021Article
- Oxidative Stress Evaluation in Ischemia Reperfusion Models: Characteristics, Limits and Perspectives.International journal of molecular sciences · 2021Review
- Sex differences in solute transport along the nephrons: effects of NaAmerican journal of physiology. Renal physiology · 2020Article
- Sensing of tubular flow and renal electrolyte transport.Nature reviews. Nephrology · 2020Review
- New metallophamaceutic reduced renal injury induced by non-steroidal anti-inflammatory.Acta cirurgica brasileira · 2020Article
- A model of mitochondrial OAmerican journal of physiology. Renal physiology · 2020Article
- Functional implications of the sex differences in transporter abundance along the rat nephron: modeling and analysis.American journal of physiology. Renal physiology · 2019Article
- Solute and water transport along an inner medullary collecting duct undergoing peristaltic contractions.American journal of physiology. Renal physiology · 2019Article
- Recent advances in sex differences in kidney function.American journal of physiology. Renal physiology · 2019Article
- Sex-specific computational models of the spontaneously hypertensive rat kidneys: factors affecting nitric oxide bioavailability.American journal of physiology. Renal physiology · 2017Article
- Modeling glucose metabolism and lactate production in the kidney.Mathematical biosciences · 2017Article
- A new microscope for the kidney: mathematics.American journal of physiology. Renal physiology · 2017Article
- Modeling Glucose Metabolism in the Kidney.Bulletin of mathematical biology · 2016Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
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Abstract
The goal of this study was to investigate the effects of nitric oxide (NO)-mediated vasodilation in preventing medullary hypoxia, as well as the likely pathways by which superoxide (O2(-)) conversely enhances medullary hypoxia. To do so, we expanded a previously developed mathematical model of solute transport in the renal medulla that accounts for the reciprocal interactions among oxygen (O2), NO, and O2(-) to include the vasoactive effects of NO on medullary descending vasa recta. The model represents the radial organization of the vessels and tubules, centered around vascular bundles in the outer medulla and collecting ducts in the inner medulla. Model simulations suggest that NO helps to prevent medullary hypoxia both by inducing vasodilation of the descending vasa recta (thus increasing O2 supply) and by reducing the active sodium transport rate (thus reducing O2 consumption). That is, the vasodilative properties of NO significantly contribute to maintaining sufficient medullary oxygenation. The model further predicts that a reduction in tubular transport efficiency (i.e., the ratio of active sodium transport per O2 consumption) is the main factor by which increased O2(-) levels lead to hypoxia, whereas hyperfiltration is not a likely pathway to medullary hypoxia due to oxidative stress. Finally, our results suggest that further increasing the radial separation between vessels and tubules would reduce the diffusion of NO towards descending vasa recta in the inner medulla, thereby diminishing its vasoactive effects therein and reducing O2 delivery to the papillary tip.
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