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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
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Nitric oxide production by glomerular podocytes.

Oleg Palygin1, Daria V Ilatovskaya1, Vladislav Levchenko1

  • 1Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.

Nitric Oxide : Biology and Chemistry
|November 13, 2017
PubMed
Summary
This summary is machine-generated.

Hypertension impairs nitric oxide (NO) production in kidney podocytes, crucial cells for filtration. This dysfunction in NO signaling contributes to kidney damage and proteinuria in salt-sensitive hypertension.

Keywords:
Angiotensin IIDAF-FMDahl salt-sensitive ratHydrogen peroxideHypertensionNitric oxide

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Area of Science:

  • Nephrology
  • Cardiovascular Research
  • Cellular Signaling

Background:

  • Nitric Oxide (NO) regulates glomerular ultrafiltration.
  • The role of NO in podocytes during salt-sensitive hypertension is not well understood.
  • Podocyte dysfunction contributes to kidney injury and proteinuria.

Purpose of the Study:

  • To investigate NO production in podocytes during salt-sensitive hypertension.
  • To determine if reduced NO production in podocytes contributes to glomerular damage and proteinuria.

Main Methods:

  • Isolated glomeruli from Dahl salt-sensitive (SS) rats on low salt (LS) or high salt (HS) diets.
  • Loaded podocytes with NO and Ca2+ fluorophores.
  • Measured NO and Ca2+ responses to ATP, Ang II, and H2O2 using confocal microscopy.

Main Results:

  • Angiotensin II (Ang II) activated both NO and intracellular calcium ([Ca2+]i) in podocytes.
  • Adenosine triphosphate (ATP) increased [Ca2+]i but not NO production.
  • Podocytes from HS-fed SS rats showed significantly reduced NO production in response to Ang II or H2O2 compared to LS-fed rats.

Conclusions:

  • Glomerular podocytes produce NO.
  • Hypertensive rats exhibit diminished NO release from podocytes in response to Ang II or oxidative stress.
  • Podocytic NO signaling is dysfunctional in salt-sensitive hypertension, contributing to kidney injury.