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10.1152/ajprenal.00583.2014 http://scihub22266oqcxt.onion/10.1152/ajprenal.00583.2014 C4346749!4346749 !25503735     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25503735 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Am+J+Physiol+Renal+Physiol 2015 ; 308 (5 ): F444-9 Nephropedia Template TP {{tp|p=25503735 |t=2015. Endogenous flow-induced nitric oxide reduces superoxide-stimulated Na/H exchange activity via PKG in thick ascending limbs |pdf=|usr=}}{{25503735 }} gab.com Text Endogenous flow-induced nitric oxide reduces superoxide-stimulated Na/H exchange activity via PKG in thick ascending limbs JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25503735 #FOAvip Luminal flow stimulates endogenous nitric oxide (NO) and superoxide (O2 (-)) production by renal thick ascending limbs (TALs). The delicate balance between these two factors regulates Na transport in TALs; NO enhances natriuresis, whereas O2 (-) augments Na absorption. Endogenous, flow-stimulated O2 (-) enhances Na/H exchange (NHE). Flow-stimulated NO reduces flow-induced O2 (-), a process mediated by cGMP-dependent protein kinase (PKG). However, whether flow-stimulated, endogenously-produced NO diminishes O2 (-)-stimulated NHE activity and the signaling pathway involved are unknown. We hypothesized that flow-induced NO reduces the stimulation of NHE activity caused by flow-induced O2 (-) via PKG in TALs. Intracellular pH recovery after an acid load was measured as an indicator of NHE activity in isolated, perfused rat TALs. l-Arginine, the NO synthase substrate, decreased NHE activity by 34 ± 5% (n = 5; P < 0.04). The O2 (-) scavenger tempol decreased NHE activity by 46 ± 8% (n = 6; P < 0.004) in the absence of NO. In the presence of l-arginine, the inhibitory effect of tempol on NHE activity was reduced to -19 ± 6% (n = 6; P < 0.03). The soluble guanylate cyclase inhibitor LY-83583 blocked the effect of l-arginine thus restoring tempol's effect on NHE activity to -42 ± 4% (n = 6; P < 0.0005). The PKG inhibitor KT-5823 also inhibited l-arginine's effect on tempol-reduced NHE activity (-43 ± 5%; n = 5; P < 0.03). We conclude that flow-induced NO reduces the stimulatory effect of endogenous, flow-induced O2 (-) on NHE activity in TALs via an increase in cGMP and PKG activation. Twit Text FOAVip Endogenous flow-induced nitric oxide reduces superoxide-stimulated Na/H exchange activity via PKG in thick ascending limbs ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25503735 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25503735 #FOAvip English Wikipedia <ref>{{Cite pmid|25503735 }}</ref> Endogenous flow-induced nitric oxide reduces superoxide-stimulated Na/H exchange activity via PKG in thick ascending limbs #MMPMID25503735 Hong NJ ; Garvin JL Am J Physiol Renal Physiol 2015[Mar]; 308 (5 ): F444-9 PMID25503735 show ga Luminal flow stimulates endogenous nitric oxide (NO) and superoxide (O2 (-)) production by renal thick ascending limbs (TALs). The delicate balance between these two factors regulates Na transport in TALs; NO enhances natriuresis, whereas O2 (-) augments Na absorption. Endogenous, flow-stimulated O2 (-) enhances Na/H exchange (NHE). Flow-stimulated NO reduces flow-induced O2 (-), a process mediated by cGMP-dependent protein kinase (PKG). However, whether flow-stimulated, endogenously-produced NO diminishes O2 (-)-stimulated NHE activity and the signaling pathway involved are unknown. We hypothesized that flow-induced NO reduces the stimulation of NHE activity caused by flow-induced O2 (-) via PKG in TALs. Intracellular pH recovery after an acid load was measured as an indicator of NHE activity in isolated, perfused rat TALs. l-Arginine, the NO synthase substrate, decreased NHE activity by 34 ± 5% (n = 5; P < 0.04). The O2 (-) scavenger tempol decreased NHE activity by 46 ± 8% (n = 6; P < 0.004) in the absence of NO. In the presence of l-arginine, the inhibitory effect of tempol on NHE activity was reduced to -19 ± 6% (n = 6; P < 0.03). The soluble guanylate cyclase inhibitor LY-83583 blocked the effect of l-arginine thus restoring tempol's effect on NHE activity to -42 ± 4% (n = 6; P < 0.0005). The PKG inhibitor KT-5823 also inhibited l-arginine's effect on tempol-reduced NHE activity (-43 ± 5%; n = 5; P < 0.03). We conclude that flow-induced NO reduces the stimulatory effect of endogenous, flow-induced O2 (-) on NHE activity in TALs via an increase in cGMP and PKG activation. |Aminoquinolines [MESH] |Animals [MESH] |Arginine [MESH] |Carbazoles [MESH] |Cyclic GMP-Dependent Protein Kinases/*metabolism [MESH] |Cyclic N-Oxides [MESH] |Hydrogen-Ion Concentration [MESH] |Loop of Henle/*metabolism [MESH] |Male [MESH] |Nitric Oxide/*metabolism [MESH] |Rats, Sprague-Dawley [MESH] |Signal Transduction [MESH] |Sodium-Hydrogen Exchangers/*metabolism [MESH] |Spin Labels [MESH]Endogenous flow-induced nitric oxide reduces superoxide-stimulated Na/(epmc).pdf DeepDyve Pubget Overpricing