Zobrazeno 1 - 10
of 108
pro vyhledávání: '"William J. Arendshorst"'
Autor:
Mark D. Stevenson, Aleksandr E. Vendrov, Xi Yang, Yuenmu Chen, Hernán A. Navarro, Nicholas Moss, Marschall S. Runge, William J. Arendshorst, Nageswara R. Madamanchi
Publikováno v:
American Journal of Physiology-Renal Physiology. 324:F335-F352
Renal reactivity to angiotensin II (ANG II) is mediated by superoxide signaling produced by NADPH oxidase (NOX)A1/NOX1. Acute vasoconstriction of renal arteries by ANG was blunted in Noxa1−/− compared with wild-type mice. NOXA1/NOX1/O2•− sign
Autor:
Elena Mironova, Crystal R. Archer, Aleksandr E. Vendrov, Marschall S. Runge, Nageswara R. Madamanchi, William J. Arendshorst, James D. Stockand, Tarek Mohamed Abd El-Aziz
Publikováno v:
American journal of physiology. Renal physiology. 323(6)
Activity of the epithelial Na+ channel (ENaC) in the distal nephron fine-tunes renal Na+ excretion. Angiotensin II (ANG II) has been reported to enhance ENaC activity. Emerging evidence suggests that NADPH oxidase (NOX) signaling plays an important r
Autor:
Hua Pan, William J. Arendshorst, Nicolas Mass, NA Holland, Mark D Stevenson, Xi Yang, James D. Stockand, Nageswara R. Madamanchi, Andrey Lozhkin, Aleksandr E. Vendrov, Marschall S. Runge, Samuel A. Wickline, Takayuki Hayami
Publikováno v:
Antioxid Redox Signal
AIMS: NADPH oxidase (NOX)-derived reactive oxygen species (ROS) are implicated in the pathophysiology of hypertension in chronic kidney disease patients. Genetic deletion of NOX activator 1 (Noxa1) subunit of NOX1 decreases ROS under pathophysiologic
Autor:
Mehmet Kesimer, Jerome Carpenter, Juliana I. Sesma, Boris Reidel, Patrick J. Moore, Alaina L. Garland, Robert Tarran, Christine S. Kim, Juan R. Sabater, David W. Scott, Scott H. Randell, Robert C. Fellner, William J. Arendshorst, William M. Abraham, Shawn T Terryah, Saira Ahmad
Publikováno v:
American Journal of Physiology-Lung Cellular and Molecular Physiology. 314:L192-L205
In cystic fibrosis (CF) lungs, epithelial Na+ channel (ENaC) hyperactivity causes a reduction in airway surface liquid volume, leading to decreased mucocilliary clearance, chronic bacterial infection, and lung damage. Inhibition of ENaC is an attract
Publikováno v:
American Journal of Physiology-Renal Physiology. 310:F832-F845
Renal blood flow autoregulation was investigated in anesthetized C57Bl6 mice using time- and frequency-domain analyses. Autoregulation was reestablished by 15 s in two stages after a 25-mmHg step increase in renal perfusion pressure (RPP). The renal
Autor:
Daniel W. Trott, Annet Kirabo, Salim R. Thabet, Meena S. Madhur, Hana A. Itani, Mohamed A. Saleh, William J. Arendshorst, Chung I. Li, David G. Harrison, Allison E. Norlander, Yu Shyr, Wei Chen, Jing Wu, Anna E. Goldstein
Publikováno v:
Hypertension. 64:1108-1115
Recent studies have emphasized a role of adaptive immunity, and particularly T cells, in the genesis of hypertension. We sought to determine the T-cell subtypes that contribute to hypertension and renal inflammation in angiotensin II–induced hypert
Publikováno v:
American Journal of Physiology-Renal Physiology. 306:F1143-F1154
Renal blood flow (RBF) responses to arginine vasopressin (AVP) were tested in anesthetized wild-type (WT) and CD38−/− mice that lack the major calcium-mobilizing second messenger cyclic ADP ribose. AVP (3–25 ng) injected intravenously produced
Publikováno v:
American Journal of Physiology-Renal Physiology. 305:F830-F838
The present renal hemodynamic study tested the hypothesis that CD38 and superoxide anion (O2·−) participate in the vasoconstriction produced by activation of thromboxane prostanoid (TP) receptors in the mouse kidney. CD38 is the major mammalian AD
The enzyme ADP-ribosyl (ADPR) cyclase plays a significant role in mediating increases in renal afferent arteriolar cytosolic calcium concentration ([Ca2+]i) in vitro and renal vasoconstriction in vivo. ADPR cyclase produces cyclic ADP ribose, a secon
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4e31261e9179267b8bbc096ec5a6c1cc
https://ora.ox.ac.uk/objects/uuid:6b0cd532-54e2-40ed-94f0-24bb08ce986b
https://ora.ox.ac.uk/objects/uuid:6b0cd532-54e2-40ed-94f0-24bb08ce986b