Christopher S. Wilcox

ORCID: 0000-0003-0943-1037
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About
Contact & Profiles
Research Areas
  • Nitric Oxide and Endothelin Effects
  • Renin-Angiotensin System Studies
  • Eicosanoids and Hypertension Pharmacology
  • Renal function and acid-base balance
  • Blood Pressure and Hypertension Studies
  • Hormonal Regulation and Hypertension
  • Electrolyte and hormonal disorders
  • Renal and Vascular Pathologies
  • Ion Transport and Channel Regulation
  • Receptor Mechanisms and Signaling
  • Acute Kidney Injury Research
  • Potassium and Related Disorders
  • Sodium Intake and Health
  • Heart Failure Treatment and Management
  • Inflammatory mediators and NSAID effects
  • Dialysis and Renal Disease Management
  • Chronic Kidney Disease and Diabetes
  • Cardiovascular Disease and Adiposity
  • Advanced Glycation End Products research
  • Heme Oxygenase-1 and Carbon Monoxide
  • Birth, Development, and Health
  • Heart Rate Variability and Autonomic Control
  • Diabetes Treatment and Management
  • Neuroscience of respiration and sleep
  • HIV-related health complications and treatments

Georgetown University
2016-2025

Hypertension Institute
2002-2024

Yale University
1982-2024

Georgetown University Medical Center
2013-2023

MedStar Georgetown University Hospital
2020-2023

St Christopher's Hospice
2012-2018

Children's National
2010-2017

Zhejiang University
2015-2017

George Washington University
2017

Uppsala University
2010-2015

Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of hospitalization for heart failure or death from cardiovascular causes among patients with stable failure. However, safety and efficacy SGLT2 when initiated soon after an episode decompensated are unknown.We performed a multicenter, double-blind trial in which type diabetes mellitus who were recently hospitalized worsening randomly assigned to receive sotagliflozin placebo. The primary end point was total number deaths...

10.1056/nejmoa2030183 article EN New England Journal of Medicine 2020-11-17

Micropuncture studies have shown that glomerular filtration rate (GFR) falls in response to a rise Na+ or Cl- concentrations the loop of Henle, whereas isolated kidneys GFR osmotic diuresis. To define separate effects an acute increase plasma sodium (PNa), chloride (PCl) osmolality (Posmol), changes renal blood flow (RBF) and were measured during intrarenal infusions hypertonic NaCl, NaHCO3, Na acetate, dextrose, NH4Cl NH4acetate denervated kidneys. The raised Posmol at experimental kidney...

10.1172/jci110820 article EN Journal of Clinical Investigation 1983-03-01

Tubular-fluid reabsorption by specialized cells of the nephron at junction ascending limb loop Henle and distal convoluted tubule, termed macula densa, releases compounds causing vasoconstriction adjacent afferent arteriole. Activation this tubuloglomerular feedback response reduces glomerular capillary pressure and, hence, filtration rate. The functions in a negative-feedback mode to relate tubular-fluid delivery reabsorption. This system has been implicated renal autoregulation, renin...

10.1073/pnas.89.24.11993 article EN Proceedings of the National Academy of Sciences 1992-12-15

Superoxide radical (O2-) is increased in the vessel wall of spontaneously hypertensive rats (SHR) where its blockade potentiates endothelium-dependent vasodilation. The purpose this study was to determine role O2- hypertension and renal vasoconstriction SHR interaction with nitric oxide (NO). Baseline mean arterial pressure (MAP) vascular resistance were markedly elevated (n=6) compared Wistar-Kyoto (WKY; n=6) (145+/-4 versus 118+/-4 mmHg, P<0.05, 24+/-3 17+/-1 mmHg x mL(-1) min(-1),...

10.1161/01.hyp.32.1.59 article EN Hypertension 1998-07-01

Phagocytes generate superoxide anion (O 2 − ) by a classic, 5-component NADPH oxidase. O contributes to hypertension in spontaneously hypertensive rats (SHR). Therefore, we tested the hypothesis that oxidase expression is enhanced SHR kidney. We also analyzed localization of components Renal was quantified reverse transcription-polymerase chain reaction and Western blotting localized Wistar Kyoto rat (WKY) kidney immunohistochemistry. The mRNA for 5 subunits phagocyte oxidase, MOX1 RENOX...

10.1161/hy0202.103264 article EN Hypertension 2002-02-01

Abstract —8-Iso prostaglandin F 2α (8-ISO) is formed nonenzymatically from the attack of superoxide radical on arachidonic acid. Therefore, 8-ISO a marker oxidative stress in vivo. We have recently shown that short-term administration membrane-permeable, metal-independent dismutase mimetic tempol (4-hydroxy-2, 2, 6, 6-tetramethyl piperidinoxyl) normalizes blood pressure spontaneously hypertensive rats (SHR). The present study was designed to test whether prolonged ameliorates and...

10.1161/01.hyp.33.1.424 article EN Hypertension 1999-01-01

HomeCirculationVol. 104, No. 16Renal Considerations in Angiotensin Converting Enzyme Inhibitor Therapy

10.1161/hc4101.096153 article EN Circulation 2001-10-16

Oxidative stress accompanies angiotensin (ANG) II infusion, but the role of ANG type 1 vs. 2 receptors (AT -R and AT -R, respectively) is unknown. We infused subcutaneously in rats for wk. Excretion 8-isoprostaglandin F α (8-Iso) malonyldialdehyde (MDA) were related to renal cortical mRNA abundance subunits NADPH oxidase superoxide dismutases (SODs) using real-time PCR. Subsets II-infused given antagonist candesartan cilexetil (Cand) or PD-123,319 (PD). Compared vehicle (Veh), increased...

10.1152/ajpregu.00476.2002 article EN AJP Regulatory Integrative and Comparative Physiology 2003-07-01

The hypothesis that a high salt (HS) intake increases oxidative stress was investigated and related to renal cortical expression of NAD(P)H oxidase superoxide dismutase (SOD). 8-Isoprostane PGF(2alpha) malonyldialdehyde were measured in groups (n = 6 8) conscious rats during low-salt, normal-salt, or HS diets. NADPH- NADH-stimulated anion (O(2)(.-)) generation assessed by chemiluminescence, SOD with real-time PCR. Excretion 8-isoprostane increased incrementally two- threefold (P < 0.001),...

10.1097/01.asn.0000092145.90389.65 article EN Journal of the American Society of Nephrology 2003-11-01
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