C
Christopher S. Wilcox
Researcher at Georgetown University
Publications - 264
Citations - 16645
Christopher S. Wilcox is an academic researcher from Georgetown University. The author has contributed to research in topics: Angiotensin II & Kidney. The author has an hindex of 64, co-authored 245 publications receiving 14929 citations. Previous affiliations of Christopher S. Wilcox include University of Tokyo & NewYork–Presbyterian Hospital.
Papers
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Journal ArticleDOI
Sotagliflozin in Patients with Diabetes and Recent Worsening Heart Failure
Deepak L. Bhatt,Michael Szarek,P. Gabriel Steg,Christopher P. Cannon,Lawrence A. Leiter,Darren K. McGuire,Julia B. Lewis,Matthew C. Riddle,Adriaan A. Voors,Marco Metra,Lars H. Lund,Michel Komajda,Jeffrey M. Testani,Christopher S. Wilcox,Piotr Ponikowski,Renato D. Lopes,Subodh Verma,Pablo Lapuerta,Bertram Pitt +18 more
TL;DR: In patients with diabetes and recent worsening heart failure, sotagliflozin therapy, initiated before or shortly after discharge, resulted in a significantly lower total number of deaths from cardiovascular causes and hospitalizations and urgent visits for heart failure than placebo.
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Nitric oxide synthase in macula densa regulates glomerular capillary pressure
Christopher S. Wilcox,William J. Welch,Ferid Murad,Steven S. Gross,Graham P. Taylor,Roberto Levi,Harald H.H.W. Schmidt +6 more
TL;DR: It is concluded that nitric oxide synthase in macula densa cells is activated by tubular-fluid reabsorption and mediates a vasodilating component to the tubuloglomerular feedback response.
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Normalization of Blood Pressure and Renal Vascular Resistance in SHR With a Membrane-Permeable Superoxide Dismutase Mimetic: Role of Nitric Oxide
TL;DR: The data implicate O2- in the hypertension of SHR in vivo and suggest that the antihypertensive action of tempol depends on NO synthesis presumably because O 2- inactivates NO and thus diminishes its vasodilatory actions.
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Oxidative stress and nitric oxide deficiency in the kidney: a critical link to hypertension?
TL;DR: ROS can diminish the efficiency with which the kidney uses O(2) for Na(+) transport and thereby diminish the P(O(2)) within the kidney cortex, which could further enhance vasculopathy and hypertension.
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NADPH oxidases in the kidney.
TL;DR: Experimental studies of the distribution, signaling, and function of NADPH oxidases in the kidney are described, with a prominent expression in renal vessels, glomeruli, and podocytes.