Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

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.

10.1161/HYPERTENSIONAHA.115.05255 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.115.05255 C4393374!4393374!25733244     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hypertension 2015 ; 65 (5): 1064-72 Nephropedia Template TP {{tp|p=25733244|t=2015. Transcriptional Regulation of Renal Dopamine D1 Receptor Function during oxidative stress |pdf=|usr=}}{{25733244}} gab.com Text Transcriptional Regulation of Renal Dopamine D1 Receptor Function during oxidative stress JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25733244 #FOAvip There exists a strong link between oxidative stress, renal dopaminergic system and hypertension. It is reported that reactive oxygen species attenuate renal proximal tubular dopamine receptor (D1R) function which disrupts sodium regulation and leads to hypertension. The mechanisms for renal D1R dysfunction however are not clear. We investigated the role of redox sensitive transcription factors AP1 and SP3 in transcriptional suppression of D1R gene and subsequent D1R signaling. Human kidney (HK2) proximal tubular cells were treated with a pro-oxidant L-buthionine sulfoximine (BSO) with and without an antioxidant tempol. In HK2 cells BSO caused oxidative stress and reduced D1R mRNA and membrane receptor expression. Incubation of HK2 cells with SKF38393, a D1R agonist, caused a concentration dependent inhibition of Na/K-ATPase. However, SKF38393 failed to inhibit Na/K-ATPase in BSO-treated cells. BSO increased AP1 and SP3 nuclear expression. Transfection with AP1 or SP3 specific siRNA abolished BSO-induced D1R down-regulation. Treatment of rats with BSO for 4 weeks increased oxidative stress and SP3?AP1 expression and reduced D1R numbers in renal proximal tubules. These rats exhibited high blood pressure and SKF38393 failed to inhibit proximal tubular Na/K-ATPase activity. Control rats were kept on tap water. Tempol per se had no effect on D1R expression or other signaling molecules but prevented BSO-induced oxidative stress, SP3?AP1 up-regulation and D1R dysfunction in both HK2 cells and rats. These data shows that oxidative stress via AP1?SP3 activation suppresses D1R transcription and function. Tempol mitigates oxidative stress, blocks AP1?SP3 activation and prevents D1R dysfunction and hypertension. Twit Text FOAVip Transcriptional Regulation of Renal Dopamine D1 Receptor Function during oxidative stress ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25733244 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25733244 #FOAvip English Wikipedia <ref>{{Cite pmid|25733244}}</ref> Transcriptional Regulation of Renal Dopamine D1 Receptor Function during oxidative stress #MMPMID25733244 Banday AA; Lokhandwala MF Hypertension 2015[May]; 65 (5): 1064-72 PMID25733244show ga There exists a strong link between oxidative stress, renal dopaminergic system and hypertension. It is reported that reactive oxygen species attenuate renal proximal tubular dopamine receptor (D1R) function which disrupts sodium regulation and leads to hypertension. The mechanisms for renal D1R dysfunction however are not clear. We investigated the role of redox sensitive transcription factors AP1 and SP3 in transcriptional suppression of D1R gene and subsequent D1R signaling. Human kidney (HK2) proximal tubular cells were treated with a pro-oxidant L-buthionine sulfoximine (BSO) with and without an antioxidant tempol. In HK2 cells BSO caused oxidative stress and reduced D1R mRNA and membrane receptor expression. Incubation of HK2 cells with SKF38393, a D1R agonist, caused a concentration dependent inhibition of Na/K-ATPase. However, SKF38393 failed to inhibit Na/K-ATPase in BSO-treated cells. BSO increased AP1 and SP3 nuclear expression. Transfection with AP1 or SP3 specific siRNA abolished BSO-induced D1R down-regulation. Treatment of rats with BSO for 4 weeks increased oxidative stress and SP3?AP1 expression and reduced D1R numbers in renal proximal tubules. These rats exhibited high blood pressure and SKF38393 failed to inhibit proximal tubular Na/K-ATPase activity. Control rats were kept on tap water. Tempol per se had no effect on D1R expression or other signaling molecules but prevented BSO-induced oxidative stress, SP3?AP1 up-regulation and D1R dysfunction in both HK2 cells and rats. These data shows that oxidative stress via AP1?SP3 activation suppresses D1R transcription and function. Tempol mitigates oxidative stress, blocks AP1?SP3 activation and prevents D1R dysfunction and hypertension. äTranscriptional Regulation of Renal Dopamine D1 Receptor Function duri(epmc).pdf DeepDyve Pubget Overpricing