Tumor necrosis factor α down-regulates the Na+–K+ ATPase and the Na+-K+2Cl− cotransporter in the kidney cortex and medulla

Kreydiyyeh, Sawsan Ibrahim; Markossian, Sarine

doi:10.1016/j.cyto.2005.12.007

Cited by 19 publications

(15 citation statements)

References 42 publications

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“…The present findings indicate that TNF-␣ exerts natriuresis via a direct action on the renal tubules as noted in the marked increase in FE Na (Table 1 and (23). In another in vitro study (2), TNF-␣ was shown to inhibit the renal epithelial sodium channel (ENaC) activity which was mediated by a PKC-dependent pathway.…”

Section: Discussionmentioning

confidence: 80%

Involvement of tumor necrosis factor-α in natriuretic response to systemic infusion of nitric oxide synthase inhibitor in anesthetized mice

Shahid

Francis

Matrougui

et al. 2010

American Journal of Physiology-Renal Physiology

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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-␣ 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 g·min Ϫ1 ·g body wt Ϫ1 for 85 min) and its impact on the plasma level of TNF-␣ were evaluated in anesthetized mice. Plasma TNF-␣ was undetected in untreated mice (n ϭ 7) but was elevated in L-NAME-treated mice (109 Ϯ 22 pg/ml; P Ͻ 0.01 vs. untreated group; n ϭ 7) along with an increase in TNF-␣ protein expression in kidney tissue. L-NAME infusion caused a usual increase in mean arterial pressure (MAP; 98 Ϯ 3 to 122 Ϯ 3 mmHg; P Ͻ 0.01) and decreases in renal blood flow (RBF; 8.6 Ϯ 0.3 to 4.4 Ϯ 0.2 ml · min Ϫ1 ·g Ϫ1 ; P Ͻ 0.01) and glomerular filtration rate (GFR; 1.14 Ϯ 0.07 to 0.77 Ϯ 0.04 ml · min Ϫ1 ·g Ϫ1 ; P Ͻ 0.01) with a marked increase in sodium excretion (U NaV; 0.48 Ϯ 0.10 to 3.52 Ϯ 0.85 mol · min Ϫ1 ·g Ϫ1 ; P Ͻ 0.01). Interestingly, in mice (n ϭ 7) pretreated with the TNF-␣ blocker etanercept (5 mg/kg sc), the U NaV response to L-NAME infusion was markedly blunted (0.58 Ϯ 0.08 to 1.22 Ϯ 0.28 mol · min Ϫ1 ·g Ϫ1 ; P ϭ NS) although responses for MAP, RBF, and GFR were mostly unchanged. However, pretreatment with the superoxide scavenger tempol in mice (n ϭ 7) did not alter the U NaV response to L-NAME. These data demonstrate that L-NAME-induced natriuresis is mediated, at least in part, by concomitant generation of TNF-␣ during NO blockade.

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Section: Discussionmentioning

confidence: 80%

Involvement of tumor necrosis factor-α in natriuretic response to systemic infusion of nitric oxide synthase inhibitor in anesthetized mice

Shahid

Francis

Matrougui

et al. 2010

American Journal of Physiology-Renal Physiology

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“…The responses to TNF-␣ in TNF␣R2 KO mice were qualitatively identical to those in WT mice. It was reported in previous in vitro studies that TNF-␣ exerts direct inhibitory action on Na (25), and epithelial sodium channel activity (2) in the renal tubule. As shown in our earlier experiments (27,32), this diuretic and natriuretic response to TNF-␣ was prevented in mice pretreated with amiloride, indicating that this natriuretic response was mediated by inhibitory action of TNF-␣ on tubular epithelial sodium channel activity.…”

mentioning

confidence: 99%

Tumor necrosis factor-α receptor type 1, not type 2, mediates its acute responses in the kidney

Castillo

Islam

Prieto

et al. 2012

American Journal of Physiology-Renal Physiology

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Acute administration of tumor necrosis factor-α (TNF-α) resulted in decreases in renal blood flow (RBF) and glomerular filtration rate (GFR) but induced diuretic and natriuretic responses in mice. To define the receptor subtypes involved in these renal responses, experiments were conducted to assess the responses to human recombinant TNF-α (0.3 ng·min−1·g body wt−1iv infusion for 75 min) in gene knockout (KO) mice for TNF-α receptor type 1 (TNFαR1 KO, n = 5) or type 2 (TNFαR2 KO, n = 6), and the results were compared with those obtained in corresponding wild-type [WT (C57BL/6), n = 6] mice. Basal levels of RBF (PAH clearance) and GFR (inulin clearance) were similar in TNFαR1 KO, but were lower in TNFαR2 KO, than WT mice. TNF-α infusion in WT mice decreased RBF and GFR but caused a natriuretic response, as reported previously. In TNFαR1 KO mice, TNF-α infusion failed to cause such vasoconstrictor or natriuretic responses; rather, there was an increase in RBF and a decrease in renal vascular resistance. Similar responses were also observed with infusion of murine recombinant TNF-α in TNFαR1 KO mice ( n = 5). However, TNF-α infusion in TNFαR2 KO mice caused changes in renal parameters qualitatively similar to those observed in WT mice. Immunohistochemical analysis in kidney slices from WT mice demonstrated that while both receptor types were generally located in the renal vascular and tubular cells, only TNFαR1 was located in vascular smooth muscle cells. There was an increase in TNFαR1 immunoreactivity in TNFαR2 KO mice, and vice versa, compared with WT mice. Collectively, these functional and immunohistological findings in the present study demonstrate that the activation of TNFαR1, not TNFαR2, is mainly involved in mediating the acute renal vasoconstrictor and natriuretic actions of TNF-α.

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“…-ATPase [16]. It also reduced protein expression of NKCC [16]. IFN-c, as well as IL-1b and TNF-a, suppressed gene expression of various transporters, including Na ?…”

Section: Implication Of the Cytokine-mediated K 1 Channel Modulation mentioning

confidence: 95%

“…channels, effects of cytokines on renal transporters are relatively well documented [10,[12][13][14][15][16][17][36][37][38]. Most of these investigations revealed the suppressive effects of cytokines on renal tubular transport [10, 12-14, 16, 17, 36-38].…”

Section: Implication Of the Cytokine-mediated K 1 Channel Modulation mentioning

confidence: 98%

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Effects of cytokines on potassium channels in renal tubular epithelia

2011

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Renal tubular potassium (K(+)) channels play important roles in the formation of cell-negative potential, K(+) recycling, K(+) secretion, and cell volume regulation. In addition to these physiological roles, it was reported that changes in the activity of renal tubular K(+) channels were involved in exacerbation of renal cell injury during ischemia and endotoxemia. Because ischemia and endotoxemia stimulate production of cytokines in immune cells and renal tubular cells, it is possible that cytokines would affect K(+) channel activity. Although the regulatory mechanisms of renal tubular K(+) channels have extensively been studied, little information is available about the effects of cytokines on these K(+) channels. The first report was that tumor necrosis factor acutely stimulated the single channel activity of the 70 pS K(+) channel in the rat thick ascending limb through activation of tyrosine phosphatase. Recently, it was also reported that interferon-γ (IFN-γ) and interleukin-1β (IL-1β) modulated the activity of the 40 pS K(+) channel in cultured human proximal tubule cells. IFN-γ exhibited a delayed suppression and an acute stimulation of K(+) channel activity, whereas IL-1β acutely suppressed the channel activity. Furthermore, these cytokines suppressed gene expression of the renal outer medullary potassium channel. The renal tubular K(+) channels are functionally coupled to the coexisting transporters. Therefore, the effects of cytokines on renal tubular transporter activity should also be taken into account, when interpreting their effects on K(+) channel activity.

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Tumor necrosis factor α down-regulates the Na+–K+ ATPase and the Na+-K+2Cl− cotransporter in the kidney cortex and medulla

Cited by 19 publications

References 42 publications

Involvement of tumor necrosis factor-α in natriuretic response to systemic infusion of nitric oxide synthase inhibitor in anesthetized mice

Involvement of tumor necrosis factor-α in natriuretic response to systemic infusion of nitric oxide synthase inhibitor in anesthetized mice

Tumor necrosis factor-α receptor type 1, not type 2, mediates its acute responses in the kidney

Effects of cytokines on potassium channels in renal tubular epithelia

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