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A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.14814/phy2.12766 http://scihub22266oqcxt.onion/10.14814/phy2.12766 C4831332!4831332 !27081160     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27081160 &cmd=llinks): Failed to open stream: HTTP request failed! 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Enhancement in cellular Na+K+ATPase activity by low doses of peroxynitrite in mouse renal tissue and in cultured HK2 cells |pdf=|usr=}}{{27081160 }} gab.com Text Enhancement in cellular Na+K+ATPase activity by low doses of peroxynitrite in mouse renal tissue and in cultured HK2 cells JO: Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=27081160 #FOAvip In the normal condition, endogenous formation of peroxynitrite (ONOO-) from the interaction of nitric oxide and superoxide has been suggested to play a renoprotective role. However, the exact mechanism associated with renoprotection by this radical compound is not yet clearly defined. AlthoughONOO- usually inhibits renal tubular Na(+)K(+)ATPase (NKA) activity at high concentrations (micromolar to millimolar range [?M-mM], achieved in pathophysiological conditions), the effects at lower concentrations (nanomolar range [nM], relevant in normal condition) remain unknown. To examine the direct effect ofONOO- onNKAactivity, preparations of cellular membrane fraction from mouse renal tissue and from culturedHK2 cells (human proximal tubular epithelial cell lines) were incubated for 10 and 30 min each with different concentrations ofONOO- (10 nmol/L-200 ?mol/L).NKAactivity in these samples (n = 5 in each case) was measured via a colorimetric assay capable of detecting inorganic phosphate. At high concentrations (1-200 ?mol/L),ONOO- caused dose-dependent inhibition ofNKAactivity (-3.0 ± 0.6% and -36.4 ± 1.4%). However,NKAactivity remained unchanged at 100 and 500 nmol/LONOO- concentration, but interestingly, at lower concentrations (10 and 50 nmol/L),ONOO- caused small but significant increases in theNKAactivity (3.3 ± 1.1% and 3.1 ± 0.6%). Pretreatment with aONOO- scavenger, mercaptoethylguanidine (MEG; 200 ?mol/L), prevented these biphasic responses toONOO-. This dose-dependent biphasic action ofONOO(-)onNKAactivity may implicate that this radical compound helps to maintain sodium homeostasis either by enhancing tubular sodium reabsorption under normal conditions or by inhibiting it during oxidative stress conditions. Twit Text FOAVip Enhancement in cellular Na+K+ATPase activity by low doses of peroxynitrite in mouse renal tissue and in cultured HK2 cells ????Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=27081160 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27081160 #FOAvip English Wikipedia <ref>{{Cite pmid|27081160 }}</ref> Enhancement in cellular Na+K+ATPase activity by low doses of peroxynitrite in mouse renal tissue and in cultured HK2 cells #MMPMID27081160 Maiti AK ; Islam MT ; Satou R ; Majid DS Physiol Rep 2016[Apr]; 4 (7 ): ä PMID27081160 show ga In the normal condition, endogenous formation of peroxynitrite (ONOO-) from the interaction of nitric oxide and superoxide has been suggested to play a renoprotective role. However, the exact mechanism associated with renoprotection by this radical compound is not yet clearly defined. AlthoughONOO- usually inhibits renal tubular Na(+)K(+)ATPase (NKA) activity at high concentrations (micromolar to millimolar range [?M-mM], achieved in pathophysiological conditions), the effects at lower concentrations (nanomolar range [nM], relevant in normal condition) remain unknown. To examine the direct effect ofONOO- onNKAactivity, preparations of cellular membrane fraction from mouse renal tissue and from culturedHK2 cells (human proximal tubular epithelial cell lines) were incubated for 10 and 30 min each with different concentrations ofONOO- (10 nmol/L-200 ?mol/L).NKAactivity in these samples (n = 5 in each case) was measured via a colorimetric assay capable of detecting inorganic phosphate. At high concentrations (1-200 ?mol/L),ONOO- caused dose-dependent inhibition ofNKAactivity (-3.0 ± 0.6% and -36.4 ± 1.4%). However,NKAactivity remained unchanged at 100 and 500 nmol/LONOO- concentration, but interestingly, at lower concentrations (10 and 50 nmol/L),ONOO- caused small but significant increases in theNKAactivity (3.3 ± 1.1% and 3.1 ± 0.6%). Pretreatment with aONOO- scavenger, mercaptoethylguanidine (MEG; 200 ?mol/L), prevented these biphasic responses toONOO-. This dose-dependent biphasic action ofONOO(-)onNKAactivity may implicate that this radical compound helps to maintain sodium homeostasis either by enhancing tubular sodium reabsorption under normal conditions or by inhibiting it during oxidative stress conditions. |Animals [MESH] |Cell Line [MESH] |Cell Membrane/*drug effects/enzymology [MESH] |Dose-Response Relationship, Drug [MESH] |Enzyme Activators/*pharmacology [MESH] |Enzyme Inhibitors/pharmacology [MESH] |Epithelial Cells/*drug effects/enzymology [MESH] |Free Radical Scavengers/pharmacology [MESH] |Humans [MESH] |Kidney Tubules, Proximal/*drug effects/enzymology [MESH] |Mice, Inbred C57BL [MESH] |Nitric Oxide/metabolism [MESH] |Peroxynitrous Acid/*pharmacology [MESH] |Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors/*metabolism [MESH]Enhancement in cellular Na+K+ATPase activity by low doses of peroxynit(epmc).pdf DeepDyve Pubget Overpricing