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.

suck abstract from ncbi


10.1016/j.bbadis.2010.03.001

http://scihub22266oqcxt.onion/10.1016/j.bbadis.2010.03.001
suck pdf from google scholar
20226856!3517663!20226856
unlimited free pdf from europmc20226856    free
PDF from PMC    free
html from PMC    free

suck abstract from ncbi


Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534

Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
pmid20226856      Biochim+Biophys+Acta 2010 ; 1802 (12): 1214-8
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • Endogenous ouabain in renal Na(+) handling and related diseases #MMPMID20226856
  • Manunta P; Messaggio E; Casamassima N; Gatti G; Carpini SD; Zagato L; Hamlyn JM
  • Biochim Biophys Acta 2010[Dec]; 1802 (12): 1214-8 PMID20226856show ga
  • The Na(+) pump and its Endogenous modulator Ouabain (EO) can be considered as an ancestral enzymatic system, conserved among species ranging from Drosophila to humans, related to Na handling. In this review, we examine how EO is linked with vascular function in hypertension and if it impacts the pathogenesis of heart and renal failure. Moreover, the molecular mechanism of endogenous ouabain-linked hypertension involves the sodium pump/sodium-calcium exchanger duet. Biosynthesis of EO occurs in adrenal glands and is under the control of angiotensin II, ACTH and epinephrine. Elevated concentrations of EO and in the sub-nanomolar concentration range were found to stimulate proliferation and differentiation of cardiac and smooth muscle cells. They may have a primary role in the development of cardiac dysfunction and failure. Experimental data suggest that the Na/K-ATPase alpha(2)-catalytic subunit causes EO-induced vasoconstriction. Finally, maneuvers that promote Na depletion, as diuretic therapy or reduced Na intake, raise the EO levels. Taken together, these findings suggest a key role for EO in body Na homeostasis.
  • |Adrenal Glands/metabolism/pathology[MESH]
  • |Angiotensin II/metabolism[MESH]
  • |Animals[MESH]
  • |Cell Proliferation/drug effects[MESH]
  • |Diuretics/therapeutic use[MESH]
  • |Drosophila[MESH]
  • |Epinephrine/metabolism[MESH]
  • |Heart Failure/drug therapy/*metabolism/pathology/physiopathology[MESH]
  • |Homeostasis/drug effects[MESH]
  • |Humans[MESH]
  • |Hypertension[MESH]
  • |Kidney/*metabolism/pathology/physiopathology[MESH]
  • |Myocytes, Cardiac/metabolism/pathology[MESH]
  • |Myocytes, Smooth Muscle/metabolism/pathology[MESH]
  • |Ouabain/*metabolism[MESH]
  • |Renal Insufficiency/drug therapy/*metabolism/pathology/physiopathology[MESH]
  • |Sodium-Calcium Exchanger[MESH]
  • |Sodium-Potassium-Exchanging ATPase/*metabolism[MESH]
  • |Sodium/*metabolism[MESH]


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    Linkout box