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.114.03609 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.114.03609 C4162752!4162752!24958497     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 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 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24958497.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Hypertension 2014 ; 64 (4): 801-7 Nephropedia Template TP {{tp|p=24958497|t=2014. THE CRITICAL BP THRESHOLD DEPENDENCE OF HYPERTENSIVE INJURY AND REPAIR IN A MALIGNANT NEPHROSCLEROSIS MODEL |pdf=|usr=}}{{24958497}} gab.com Text THE CRITICAL BP THRESHOLD DEPENDENCE OF HYPERTENSIVE INJURY AND REPAIR IN A MALIGNANT NEPHROSCLEROSIS MODEL JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=24958497 #FOAvip Most patients with essential hypertension do not exhibit substantial renal damage. Renal autoregulation, by preventing glomerular transmission of systemic pressures has been postulated to mediate this resistance. Conversely, malignant nephrosclerosis (MN) has been postulated to develop when severe hypertension exceeds a critical ceiling. If the concept is valid, even modest BP reductions to below this threshold regardless of antihypertensive class (i) should prevent MN and (ii) lead to the healing of the already developed MN lesions. Both predicates were tested using BP radiotelemetry in the stroke prone spontaneously hypertensive rats (SHRsp) receiving 1% NaCl as drinking fluid for 4 weeks. Severe hypertension (final 2 weeks average systolic BP, >200 mmHg) and MN (histologic damage score 36±5; n=27), developed in the untreated SHRsp but were prevented by all antihypertensive classes [enalapril (n=15), amlodipine (n=13) or a hydralazine/hydrochlorothiazide combination (n=15)], if the final 2 week systolic BP remained <190mmHg. More impressively, modest systolic BP reductions to 160?180mmHg (Hydralazine/Hydrochlorothiazide regimen) initiated at ?4 wks in additional untreated rats after MN had already developed (injury score 35±4 in the right kidney removed before therapy) led to a striking resolution of the vascular and glomerular MN injury over 2?3 weeks (post therapy left kidney injury score 9±2, p<0.0001; n=27). Proteinuria also declined rapidly from 122±9.5 mg/24 hr before therapy to 20.5±3.6mg 1 week later. These data clearly demonstrate the barotrauma mediated pathogenesis of MN and the striking capacity for spontaneous and rapid repair of hypertensive kidney damage if new injury is prevented. Twit Text FOAVip THE CRITICAL BP THRESHOLD DEPENDENCE OF HYPERTENSIVE INJURY AND REPAIR IN A MALIGNANT NEPHROSCLEROSIS MODEL ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=24958497 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24958497 #FOAvip English Wikipedia <ref>{{Cite pmid|24958497}}</ref> THE CRITICAL BP THRESHOLD DEPENDENCE OF HYPERTENSIVE INJURY AND REPAIR IN A MALIGNANT NEPHROSCLEROSIS MODEL #MMPMID24958497 Griffin KA; Polichnowski A; Litbarg N; Picken M; Venkatachalam M; Bidani AK Hypertension 2014[Oct]; 64 (4): 801-7 PMID24958497show ga Most patients with essential hypertension do not exhibit substantial renal damage. Renal autoregulation, by preventing glomerular transmission of systemic pressures has been postulated to mediate this resistance. Conversely, malignant nephrosclerosis (MN) has been postulated to develop when severe hypertension exceeds a critical ceiling. If the concept is valid, even modest BP reductions to below this threshold regardless of antihypertensive class (i) should prevent MN and (ii) lead to the healing of the already developed MN lesions. Both predicates were tested using BP radiotelemetry in the stroke prone spontaneously hypertensive rats (SHRsp) receiving 1% NaCl as drinking fluid for 4 weeks. Severe hypertension (final 2 weeks average systolic BP, >200 mmHg) and MN (histologic damage score 36±5; n=27), developed in the untreated SHRsp but were prevented by all antihypertensive classes [enalapril (n=15), amlodipine (n=13) or a hydralazine/hydrochlorothiazide combination (n=15)], if the final 2 week systolic BP remained <190mmHg. More impressively, modest systolic BP reductions to 160?180mmHg (Hydralazine/Hydrochlorothiazide regimen) initiated at ?4 wks in additional untreated rats after MN had already developed (injury score 35±4 in the right kidney removed before therapy) led to a striking resolution of the vascular and glomerular MN injury over 2?3 weeks (post therapy left kidney injury score 9±2, p<0.0001; n=27). Proteinuria also declined rapidly from 122±9.5 mg/24 hr before therapy to 20.5±3.6mg 1 week later. These data clearly demonstrate the barotrauma mediated pathogenesis of MN and the striking capacity for spontaneous and rapid repair of hypertensive kidney damage if new injury is prevented. äTHE CRITICAL BP THRESHOLD DEPENDENCE OF HYPERTENSIVE INJURY AND REPAIR(epmc).pdf DeepDyve Pubget Overpricing