Friederich-Persson 2014 Adv Exp Med Biol

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Friederich-Persson M, Welch WJ, Luo Z, Palm F, Nordquist L (2015) Angiotensin II reduces transport-dependent oxygen consumption but increases transport-independent oxygen consumption in immortalized mouse proximal tubular cells. Adv Exp Med Biol 812:157-63.

Β» PMID:24729228

Friederich-Persson M, Welch WJ, Luo Z, Palm F, Nordquist L (2015) Adv Exp Med Biol

Abstract: Oxidative stress is closely associated with renal dysfunction following diabetes and hypertension. Angiotensin II (Ang II) can activate the NADPH-oxidase, increasing oxidative stress that is thought to blunt proximal tubular electrolyte transport and thereby oxygen consumption (QOβ‚‚). We investigated the effect of Ang II on QOβ‚‚ in immortalized mouse proximal tubular cells over-expressing the NADPH oxidase subunit p22(phox); a model of increased oxidative stress. Cultured cells were exposed to either Ang II or Hβ‚‚Oβ‚‚ for 48 h. QOβ‚‚ was determined during baseline (113 mmol/l NaCl; transport-dependent QOβ‚‚) and during sodium-free conditions (transport-independent QOβ‚‚). Ang II reduced transport-dependent QOβ‚‚ in wild-types, but not in p22(phox) which also displayed increased QOβ‚‚ at baseline. Transport-independent QOβ‚‚ was increased in p22(phox) and Ang II had no additional effect, whereas it increased QOβ‚‚ in wild-type. Addition of Hβ‚‚Oβ‚‚ reduced transport-dependent QOβ‚‚ in wild-types, but not in p22(phox). Transport-independent QOβ‚‚ was unaffected by Hβ‚‚Oβ‚‚. The similar effects of Ang II and Hβ‚‚Oβ‚‚ to reduce transport-dependent QOβ‚‚ suggest a direct regulatory role of oxidative stress. In accordance, the transport-dependent QOβ‚‚ was reduced in p22(phox) already during baseline. The effects of Ang II on transport-independent QOβ‚‚ was not replicated by Hβ‚‚Oβ‚‚, indicating direct regulation via Ang II-receptors independently of oxidative stress. However, the Ang II effect was absent in p22(phox), suggesting that oxidative stress also modulates normal Ang II signaling. In conclusion, Ang II affects both transport-dependent and transport-independent QOβ‚‚ in proximal tubular cells and may be an important pathway modulating renal QOβ‚‚.


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Stress:Oxidative stress;RONS  Organism: Mouse  Tissue;cell: Kidney 





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