Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.6.1.3 (
ATPase
)
65,361
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Intracytoplasmic free calcium ions (Ca++) are maintained at a very low concentration in mammalian tissue by extruding Ca++ from the cytoplasm against a steep extracellular Ca++ concentration gradient, mainly through the activity of plasma membrane Ca++ pump-
ATPase
. The present study aimed to elucidate how endothelin-1 (ET-1) affects the morphology of sinusoidal endothelial fenestrae and ultrastructural distribution of plasma membrane ATPases and intracytoplasmic free Ca++ in isolated rat hepatic sinusoidal endothelial cells. Sinusoidal endothelial fenestrae were observed by scanning electron microscope. Ando's electron cytochemical method was used for ultrastructural localization of Ca++-Mg++-
ATPase
activity, electron immunogold postembedding method for Ca++ pump-
ATPase
immunoactivity, and antimonate method for intracytoplasmic free Ca++. Addition of ET-1 to sinusoidal endothelial cells significantly decreased Ca++-Mg++-
ATPase
activity and Ca++ pump-
ATPase
expression and increased intracytoplasmic free Ca++ concentration, concomitant with a decrease in diameter of sinusoidal endothelial fenestrae. Co-treatment with
Bosentan
abolished the actions of ET-1. These results suggest that ET-1 suppresses Ca++-Mg++-
ATPase
activity and Ca++ pump-
ATPase
expression on the plasma membrane of sinusoidal endothelial fenestrae, thereby attenuating the extrusion of intracytoplasmic free Ca++ into the extracellular space, leading to an increased concentration of intracytoplasmic free calcium ions and contraction of sinusoidal endothelial fenestrae.
...
PMID:Endothelin-1 suppresses plasma membrane Ca++-ATPase, concomitant with contraction of hepatic sinusoidal endothelial fenestrae. 1254 13
We tested the hypothesis that increased dietary protein augments distal nephron acidification through an endothelin-dependent mechanism. Munich-Wistar rats ate minimum electrolyte diets of 50% (HiPro) and 20% (CON) casein-provided protein, the latter comparable to standard chow. HiPro vs. CON had higher distal nephron H+ secretion (41.3 +/- 4.0 vs. 23.0 +/- 2.1 pmol/mm.min, p < 0.002) mediated by augmented Na+/H+ exchange and H(+)-
ATPase
activity. Renal cortex of HiPro vs. CON had higher ET-1 addition to microdialysate and higher ET-1 mRNA, consistent with increased renal ET-1 production.
Bosentan
, an endothelin A/B receptor antagonist, decreased HiPro distal nephron H+ secretion (28.4 +/- 2.4 vs. 41.3 +/- 4.0 pmol/mm.min, p < 0.016) through decreased Na+/H+ exchange and decreased H(+)-
ATPase
activity. Increased dietary protein augments distal nephron acidification through an endothelin-sensitive increase in Na+/H+ exchange and H(+)-
ATPase
activity, supporting an endothelin role in the distal nephron response to this common challenge to acid-base status.
...
PMID:Increased endothelin activity mediates augmented distal nephron acidification induced by dietary protein. 1655 18