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- W2135307140 abstract "Hypotension and shock observed in sepsis, SIRS, and tumor necrosis factor (TNF) or cytokine-based cancer treatment are the consequence of excessive nitric oxide (NO) production and subsequent soluble guanylate cyclase (sGC)-mediated vascular smooth muscle relaxation. We demonstrate here that, while NO synthase (NOS) inhibitors exacerbated toxicity, inhibitors of sGC activation protected against TNF-induced lethality, bradycardia, and hypotension. Importantly, sGC inhibition did not interfere with the antitumor activity of TNF. Using NOS inhibitors or iNOS-deficient animals, we furthermore observed that no protection against TNF toxicity could be obtained in the absence of NO. These data imply that iNOS- (and not eNOS-) derived NO is an endogenous protective molecule indispensable to survive a TNF challenge and exerting this beneficial effect via sGC-independent mechanisms." @default.
- W2135307140 created "2016-06-24" @default.
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- W2135307140 date "2000-08-01" @default.
- W2135307140 modified "2023-10-18" @default.
- W2135307140 title "Protection against TNF-Induced Lethal Shock by Soluble Guanylate Cyclase Inhibition Requires Functional Inducible Nitric Oxide Synthase" @default.
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- W2135307140 doi "https://doi.org/10.1016/s1074-7613(00)00022-4" @default.
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