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

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-a and IFN-'y. NO* production by both cell types was inhibited by NM-monomethyl-L-arginine; this inhibition was partially reversed by the addition of excess L-arginine. Stimulation of kidney epithelial cells with TNF-a and IFN-"y 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. (J. Clin. Invest. 1993. 91:2138-2143

Identification of a contractile function for renal medullary interstitial cells.

“…To examine whether NO could be modifying the ET-1 response, RMIC were preincubated with NMMA, an antagonist of NO action. The dose of NMMA used has been previously shown to completely block endogenous NO production by a number of cell types (21). NMMA had no effect on basal RMIC surface area nor did it alter ET-1 -induced contraction (Fig.…”

“…RMIC in 24-well plates were exposed to 0.1-100 nM ET-1 in KRB at 370C for 5-30 min. After incubation, duplicate 50-Ml aliquots of the supernatants were removed and immediately tested for nitrite (NO-) levels (stable breakdown product of nitric oxide) as previously described (21). To each aliquot, 100 ILI of Greiss reagent (1% sulfanilamide in 30% acetic acid and 0.1% N-(l-naphthyl)ethylenediamine dihydrochloride in 60% acetic acid in a 1:1 mixture) was added and mixed for one min.…”

Cytokines and Sodium Induce Protein Kinase A–Dependent Cell-Surface Na,K-ATPase Recruitment via Dissociation of NF-κB/IκB/Protein Kinase A Catalytic Subunit Complex in Collecting Duct Principal Cells

“…Moreover, measurement of the amiloride-sensitive Isc revealed that both LPS and TNF-␣ stimulated transepithelial Na ϩ transport in a PKA-dependent manner in cultured CD principal cells (see Figure 2). It should be mentioned that previous studies reported an inhibitory effect of cytokines (IL-1␤ and TNF-␣) and LPS on renal transepithelial Na ϩ transport (33)(34)(35). However, these reports focused on long-term effects (up to 24 h) that led to an increased expression of nitric oxide (NO) synthase, which in turn increases production of NO, a potent inhibitor of tubular Na ϩ reabsorption (36,37).…”

Potential Impact of Quercetin and Idebenone against Immuno- inflammatory and Oxidative Renal Damage Induced in Rats by Titanium Dioxide Nanoparticles Toxicity

“…Also, previous published data stated that high amounts of NO are released from the inducible NO synthase iNOS isoform in response to inflammatory stimuli from a variety of cell types 43 . Renal proximal tubule and inner medullary collecting duct cells can produce NO via expression of an inducible isoform of nitric oxide synthase 44 . Mesangial cells and invading immune cells are capable of expressing iNOS upon stimulation with TNF-α and IL-1b.…”