ArticleAmerican journal of physiology. Renal physiology2010
Involvement of tumor necrosis factor-alpha in natriuretic response to systemic infusion of nitric oxide synthase inhibitor in anesthetized mice.
Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- TRPV1 blockade restores the baroreflex control of renal sympathetic nerve activity in cisplatin-induced renal injury in rats.Experimental physiology · 2025Article
- Tumor necrosis factor-α in the mediation of acute salt loading induced natriuresis in mice; evidence for its physiological role in regulating kidney function.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Augmentation of Nitric Oxide Deficient Hypertension by High Salt Diet Is Associated With Reduced TNF-α Receptor Type 1 Expression in the Kidneys.American journal of hypertension · 2024Article
- Review
- Angiotensin II-induced renal angiotensinogen formation is enhanced in mice lacking tumor necrosis factor-alpha type 1 receptor.Physiological reports · 2021Article
- Angiotensin II-induced natriuresis is attenuated in knockout mice lacking the receptors for tumor necrosis factor-α.Physiological reports · 2021Article
- High-salt intake reduces renal tissue levels of inflammatory cytokines in mice.Physiological reports · 2021Article
- Norvaline Reduces Blood Pressure and Induces Diuresis in Rats with Inherited Stress-Induced Arterial Hypertension.BioMed research international · 2020Article
- Regulation of NKCC2B by TNF-α in response to salt restriction.American journal of physiology. Renal physiology · 2020Article
- Evidence for Prohypertensive, Proinflammatory Effect of Interleukin-10 During Chronic High Salt Intake in the Condition of Elevated Angiotensin II Level.Hypertension (Dallas, Tex. : 1979) · 2017Article
- Tumor necrosis factor-α, kidney function, and hypertension.American journal of physiology. Renal physiology · 2017Review
- Role of renal transporters and novel regulatory interactions in the TAL that control blood pressure.Physiological genomics · 2017Review
- Brazilin exerts protective effects against renal ischemia-reperfusion injury by inhibiting the NF-κB signaling pathway.International journal of molecular medicine · 2016Article
- Role of atrial natriuretic peptide in mediating the blood pressure-independent natriuresis elicited by systemic inhibition of nitric oxide.Pflugers Archiv : European journal of physiology · 2015Article
- Decrease in IL-10 and increase in TNF-α levels in renal tissues during systemic inhibition of nitric oxide in anesthetized mice.Physiological reports · 2014Article
- The cooperative roles of inflammation and oxidative stress in the pathogenesis of hypertension.Antioxidants & redox signaling · 2014Review
- Protective role of the endothelial isoform of nitric oxide synthase in ANG II-induced inflammatory responses in the kidney.American journal of physiology. Renal physiology · 2013Article
- NKCC2A and NFAT5 regulate renal TNF production induced by hypertonic NaCl intake.American journal of physiology. Renal physiology · 2013Article
- Tumor necrosis factor-alpha induces renal cyclooxygenase-2 expression in response to hypercalcemia.Prostaglandins & other lipid mediators · 2012Article
- Eicosanoids and tumor necrosis factor-alpha in the kidney.Prostaglandins & other lipid mediators · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Systemic infusion of TNF-alpha exerts renal vasoconstriction but caused marked natriuresis in mice. Similar renal responses were also observed during systemic infusion of nitric oxide (NO) synthase inhibitors as opposed to their usual antinatriuretic responses when administered intrarenally. In the present study, we examined the hypothesis that acute NO blockade systemically induces TNF-alpha generation. which induces this natriuretic response. Renal responses to intravenous infusion of the NO synthase inhibitor nitro-L-arginine methyl ester (L-NAME; 0.2 microg x min(-1) x g body wt(-1) for 85 min) and its impact on the plasma level of TNF-alpha were evaluated in anesthetized mice. Plasma TNF-alpha was undetected in untreated mice (n = 7) but was elevated in L-NAME-treated mice (109 +/- 22 pg/ml; P < 0.01 vs. untreated group; n = 7) along with an increase in TNF-alpha protein expression in kidney tissue. L-NAME infusion caused a usual increase in mean arterial pressure (MAP; 98 +/- 3 to 122 +/- 3 mmHg; P < 0.01) and decreases in renal blood flow (RBF; 8.6 +/- 0.3 to 4.4 +/- 0.2 ml x min(-1) x g(-1); P < 0.01) and glomerular filtration rate (GFR; 1.14 +/- 0.07 to 0.77 +/- 0.04 ml x min(-1) x g(-1); P < 0.01) with a marked increase in sodium excretion (U(Na)V; 0.48 +/- 0.10 to 3.52 +/- 0.85 micromol x min(-1) x g(-1); P < 0.01). Interestingly, in mice (n = 7) pretreated with the TNF-alpha blocker etanercept (5 mg/kg sc), the U(Na)V response to l-NAME infusion was markedly blunted (0.58 +/- 0.08 to 1.22 +/- 0.28 micromol x min(-1) x g(-1); P = NS) although responses for MAP, RBF, and GFR were mostly unchanged. However, pretreatment with the superoxide scavenger tempol in mice (n = 7) did not alter the U(Na)V response to L-NAME. These data demonstrate that L-NAME-induced natriuresis is mediated, at least in part, by concomitant generation of TNF-alpha during NO blockade.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.