Nitric oxide production by glomerular podocytes

Research output: Contribution to journalArticle

Authors

External Institution(s)

  • Medical College of Wisconsin

Details

Original languageEnglish (US)
Pages (from-to)24-31
Number of pages8
JournalNitric Oxide - Biology and Chemistry
Volume72
StatusPublished - Jan 30 2018
Peer-reviewedYes

Abstract

Nitric Oxide (NO), a potent vasodilator and vital signaling molecule, has been shown to contribute to the regulation of glomerular ultrafiltration. However, whether changes in NO occur in podocytes during the pathogenesis of salt-sensitive hypertension has not yet been thoroughly examined. We showed here that podocytes produce NO, and further hypothesized that hypertensive animals would exhibit reduced NO production in these cells in response to various paracrine factors, which might contribute to the damage of glomeruli filtration barrier and development of proteinuria. To test this, we isolated glomeruli from the kidneys of Dahl salt-sensitive (SS) rats fed a low salt (LS; 0.4% NaCl) or high salt (HS; 4% NaCl, 3 weeks) diets and loaded podocytes with either a combination of NO and Ca2+ fluorophores (DAF-FM and Fura Red, respectively) or DAF-FM alone. Changes in fluorescence were observed with confocal microscopy in response to adenosine triphosphate (ATP), angiotensin II (Ang II), and hydrogen peroxide (H2O2). Application of Ang II resulted in activation of both NO and intracellular calcium ([Ca2+]i) transients. In contrast, ATP promoted [Ca2+]i transients, but did not have any effects on NO production. SS rats fed a HS diet for 3 weeks demonstrated impaired NO production: the response to Ang II or H2O2 in podocytes of glomeruli isolated from SS rats fed a HS diet was significantly reduced compared to rats fed a LS diet. Therefore, glomerular podocytes from hypertensive rats showed a diminished NO release in response to Ang II or oxidative stress, suggesting that podocytic NO signaling is dysfunctional in this condition and likely contributes to the development of kidney injury.

    Research areas

  • Angiotensin II, DAF-FM, Dahl salt-sensitive rat, Hydrogen peroxide, Hypertension, Nitric oxide

Citation formats

APA

Palygin, O., Ilatovskaya, D. V., Levchenko, V., Endres, B. T., Geurts, A. M., & Staruschenko, A. (2018). Nitric oxide production by glomerular podocytes. Nitric Oxide - Biology and Chemistry, 72, 24-31. https://doi.org/10.1016/j.niox.2017.11.005

Harvard

Palygin, O, Ilatovskaya, DV, Levchenko, V, Endres, BT, Geurts, AM & Staruschenko, A 2018, 'Nitric oxide production by glomerular podocytes', Nitric Oxide - Biology and Chemistry, vol. 72, pp. 24-31. https://doi.org/10.1016/j.niox.2017.11.005