Blood flow, oxygenation, and oxidative stress in the post-stenotic kidney

Roger G. Evans, Paul M O'Connor

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Citations (Scopus)

Abstract

Renal ischemia, hypoxia and oxidative stress progress together over the course of renovascular disease, and thus appear to operate in a vicious pathological triangle. Renal ischemia is initially driven by the mechanical effect of the stenosis, and maintained in the medium term chiefly by activation of the systemic and intrarenal renin-angiotensin systems. In the longer term, ischemia is exacerbated by inflammation, fibrosis and microvascular rarefaction, at least partly driven by signaling cascades initiated by oxidative stress and tissue hypoxia. Oxidative stress in renovascular disease is initially driven by activation of the renin-angiotensin system, but other factors, such as the pro-oxidant effects of uremic toxins, likely also contribute in the longer term. Oxidative stress drives ischemia by the direct vasoconstrictor effects of reactive oxygen species such as superoxide, and through reduced bioavailability of the vasodilator nitric oxide. This microvascular dysfunction appears to be a major driver of microvascular remodeling and rarefaction. Ischemia drives tissue hypoxia by reducing oxygen delivery to tissue. Oxidative stress and the resultant reduction in nitric oxide bioavailability also promote hypoxia by reducing the efficiency of oxygen utilization in mitochondria. Reduced glomerular filtration leads to reduced renal oxygen consumption, so provides some protection against the development of tissue hypoxia, at least in mild or early stage renovascular disease. But, eventually, homeostasis of tissue oxygenation cannot be maintained, and tissue hypoxia ensues.

Original languageEnglish (US)
Title of host publicationRenal Vascular Disease
PublisherSpringer-Verlag London Ltd
Pages151-171
Number of pages21
Volume9781447128106
ISBN (Print)9781447128106, 1447128095, 9781447128090
DOIs
StatePublished - Dec 1 2014

Fingerprint

Oxidative Stress
Kidney
Ischemia
Renin-Angiotensin System
Biological Availability
Reactive Oxygen Species
Nitric Oxide
Oxygen
Vasoconstrictor Agents
Vasodilator Agents
Oxygen Consumption
Superoxides
Hypoxia
Mitochondria
Pathologic Constriction
Homeostasis
Fibrosis
Inflammation

Keywords

  • Fibrosis
  • Inflammation
  • Microvascular rarefaction
  • Oxidative stress
  • Oxygen
  • Perfusion
  • Renal cortex
  • Renal medulla

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Evans, R. G., & O'Connor, P. M. (2014). Blood flow, oxygenation, and oxidative stress in the post-stenotic kidney. In Renal Vascular Disease (Vol. 9781447128106, pp. 151-171). Springer-Verlag London Ltd. https://doi.org/10.1007/978-1-4471-2810-6_9

Blood flow, oxygenation, and oxidative stress in the post-stenotic kidney. / Evans, Roger G.; O'Connor, Paul M.

Renal Vascular Disease. Vol. 9781447128106 Springer-Verlag London Ltd, 2014. p. 151-171.

Research output: Chapter in Book/Report/Conference proceedingChapter

Evans, RG & O'Connor, PM 2014, Blood flow, oxygenation, and oxidative stress in the post-stenotic kidney. in Renal Vascular Disease. vol. 9781447128106, Springer-Verlag London Ltd, pp. 151-171. https://doi.org/10.1007/978-1-4471-2810-6_9
Evans RG, O'Connor PM. Blood flow, oxygenation, and oxidative stress in the post-stenotic kidney. In Renal Vascular Disease. Vol. 9781447128106. Springer-Verlag London Ltd. 2014. p. 151-171 https://doi.org/10.1007/978-1-4471-2810-6_9
Evans, Roger G. ; O'Connor, Paul M. / Blood flow, oxygenation, and oxidative stress in the post-stenotic kidney. Renal Vascular Disease. Vol. 9781447128106 Springer-Verlag London Ltd, 2014. pp. 151-171
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