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Research Article Free access | 10.1172/JCI116439

Cytokine-induced expression of a nitric oxide synthase in rat renal tubule cells.

B A Markewitz, J R Michael, and D E Kohan

Department of Medicine, Veterans Administration Medical Center, Salt Lake City, Utah.

Find articles by Markewitz, B. in: PubMed | Google Scholar

Department of Medicine, Veterans Administration Medical Center, Salt Lake City, Utah.

Find articles by Michael, J. in: PubMed | Google Scholar

Department of Medicine, Veterans Administration Medical Center, Salt Lake City, Utah.

Find articles by Kohan, D. in: PubMed | Google Scholar

Published May 1, 1993 - More info

Published in Volume 91, Issue 5 on May 1, 1993
J Clin Invest. 1993;91(5):2138–2143. https://doi.org/10.1172/JCI116439.
© 1993 The American Society for Clinical Investigation
Published May 1, 1993 - Version history
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Abstract

Nitric oxide (NO.) has been implicated in the regulation of renal vascular tone and tubular sodium transport. While the endothelial cell is a well known source of NO(.), recent studies suggest that tubular epithelial cells may constitutively generate NO(.). An inducible isoform of nitric oxide synthase which produces far greater quantities of NO. exists in some cell types. We sought to determine whether kidney epithelial cells exposed to cytokines could express an inducible nitric oxide synthase. Primary cultures of rat proximal tubule and inner medullary collecting duct cells generated NO. on exposure to TNF-alpha and IFN-gamma. NO. production by both cell types was inhibited by NG-monomethyl-L-arginine; this inhibition was partially reversed by the addition of excess L-arginine. Stimulation of kidney epithelial cells with TNF-alpha and IFN-gamma dramatically increased the level of inducible nitric oxide synthase mRNA. In summary, renal proximal tubule and inner medullary collecting duct cells can produce NO. via expression of an inducible isoform of nitric oxide synthase.

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