Na,K-ATPase represents the key enzyme that maintains the homeostasis of sodium and potassium ions in the cells. It was documented that in directly irradiated organs the activity of this enzyme is decreased. The aim of present study was to clarify the remote effect of irradiation in mediastinal area on the activity of the Na,K-ATPase in kidneys in rats. Ionizing radiation in single dose 25 Gy resulted in consequent decrease of the body weight gain as well as the size of kidneys in Wistar rats. In addition, radiation induced alterations in the oxidative status of blood plasma. Irradiation also decreased the activity of renal Na,K-ATPase. Measurements of enzyme kinetics that were dependent on the concentration of energy substrate ATP or cofactor Na indicated that the lowered enzyme activity is probably a consequence of decreased number of active molecules of the enzyme, as suggested by lowered V values. Immunoblot analysis confirmed the lowered expression of the catalytic alpha subunit together with decreased content of the glycosylated form of beta subunit in the renal tissue of irradiated rats. The ability of the enzyme to bind the substrate ATP, as well as Na was not affected, as shown by unaltered values of K and K . Irradiation of the body in the mediastinal area despite protection of kidneys by lead plates during application of X-ray was followed by significant decline of activity of the renal Na,K-ATPase, what may result in deteriorated homeostasis in the organism.
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http://dx.doi.org/10.14814/phy2.13969 | DOI Listing |
Life Sci
February 2020
Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, United States of America. Electronic address:
Hypertension is a risk factor for premature death and roughly 50% of hypertensive patients are salt-sensitive. The incidence of salt-sensitive hypertension increases with age. However, the mechanisms of salt-sensitive hypertension are not well understood.
View Article and Find Full Text PDFBiochim Biophys Acta
November 2016
Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA. Electronic address:
Our laboratory has recently demonstrated that low concentrations of ouabain increase blood pressure in rats associated with stimulation of NaK ATPase activity and activation of the Src signaling cascade in NHE1-dependent manner. Proteomic analysis of human kidney proximal tubule cells (HKC11) suggested that the Angiotensin II type 1 receptor (AT1R) as an ouabain-associating protein. We hypothesize that ouabain-induced stimulation of NaK ATPase activity is mediated through AT1R.
View Article and Find Full Text PDFJ Biol Chem
November 2013
Department of Pharmacology, Physiology and Toxicology, JCE School of Medicine at Marshall University, Huntington, West Virginia 25755. Electronic address:
Cardiotonic steroids (such as ouabain) signaling through Na/K-ATPase regulate sodium reabsorption in the renal proximal tubule. We report here that reactive oxygen species are required to initiate ouabain-stimulated Na/K-ATPase·c-Src signaling. Pretreatment with the antioxidant N-acetyl-L-cysteine prevented ouabain-stimulated Na/K-ATPase·c-Src signaling, protein carbonylation, redistribution of Na/K-ATPase and sodium/proton exchanger isoform 3, and inhibition of active transepithelial (22)Na(+) transport.
View Article and Find Full Text PDFJ Am Soc Nephrol
June 2004
Department of Pediatrics, Yale University, New Haven, CT 06520-8064, USA.
To test a putative cause and effect relationship between heat-shock protein (HSP) expression and response to renal cell injury, HSP72 and HSP25 were differentially inhibited in LLC-PK1 cells by means of transcription factor decoy and short interference RNA (siRNA). Cellular injury was assessed by solubilization of NaK ATPase (S-NaK). An exonuclease-resistant, ethylene glycol-bridged, circular oligonucleotide decoy for heat-shock transcription factor (HSF)-1, based on the sequence of the porcine heat-shock element, was constructed and validated.
View Article and Find Full Text PDFMinerva Urol Nefrol
December 2002
Department of Medicine, Mount Sinai School of Medicine, Box 1243, 1425 Madison Avenue, New York, NY 10029, USA.
Genetically based polycystic kidney diseases include autosomal dominant (ADPKD) and recessive (ARPKD) polycystic kidney diseases, nephronophthisis and medullary cystic disease. The PKD1 and PKD2 genes responsible for ADPKD and their respective encoded proteins polycystin-1 and polycystin-2 are under intense study and clues are developing as to their function and roles in the disease process. Structure-function analysis suggests that polycystins form multiprotein complexes with focal adhesion and cell-cell adherens junction proteins, which then initiate intracellular signaling events culminating in regulation of transcription of genes controlling proliferation and differentiation.
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