title: High-salt diet induces outward remodelling of efferent arterioles in mice with reduced renal mass.
abstract: The glomerular filtration rate (GFR) falls progressively in chronic kidney disease (CKD) which is caused by a reduction in the number of functional nephrons. The dysfunctional nephron exhibits a lower glomerular capillary pressure that is induced by an unbalance between afferent and efferent arteriole. Therefore, we tested the hypothesis that oxidative stress induced by CKD differentially impairs the structure or function of efferent vs. afferent arterioles.
  
  
  
  C57BL/6 mice received sham operations (sham) or 5/6 nephrectomy (RRM) and three months of normal- or high-salt diet or tempol. GFR was assessed from the plasma inulin clearance, arteriolar remodelling from media/lumen area ratio, myogenic responses from changes in luminal diameter with increases in perfusion pressure and passive wall compliance from the wall stress/strain relationships.
  
  
  
  Mice with RRM fed a high salt (vs. sham) had a lower GFR (553 ± 25 vs. 758 ± 36 μL min-1g-1kidney, P < 0.01) and a larger efferent arteriolar diameter (9.6 ± 0.8 vs. 7.4 ± 0.7 μm, P < 0.05) resulting in a lower media/lumen area ratio (1.4 ± 0.1 vs. 2.4 ± 0.2, P < 0.01). These alterations were corrected by tempol. The myogenic responses of efferent arterioles were about one-half that of afferent arterioles and were unaffected by RRM or salt. Passive wall compliance was reduced by high salt in both afferent and efferent arterioles.
  
  
  
  A reduction in renal mass with a high-salt diet induces oxidative stress that leads to an outward eutrophic remodelling in efferent arterioles and reduced wall compliance in both afferent and efferent arterioles. This may contribute to the lower GFR in this model of CKD.
authors.affiliation: Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China.
authors.forename: L
authors.initials: L
authors.lastname: Zhao
authors.affiliation: Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Gao
authors.affiliation: Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China.
authors.forename: X
authors.initials: X
authors.lastname: Cao
authors.affiliation: Department of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
authors.forename: D
authors.initials: D
authors.lastname: Gao
authors.affiliation: Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China.
authors.forename: S
authors.initials: S
authors.lastname: Zhou
authors.affiliation: Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China.
authors.forename: S
authors.initials: S
authors.lastname: Zhang
authors.affiliation: Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China.|Department of Basic Medicine, Honghe Health Vocational College, Mengzi, China.
authors.forename: X
authors.initials: X
authors.lastname: Cai
authors.affiliation: Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
authors.forename: F
authors.initials: F
authors.lastname: Han
authors.affiliation: Division of Nephrology and Hypertension, Hypertension, Kidney and Vascular Health Center, Georgetown University, Washington, DC, USA.
authors.forename: C S
authors.initials: CS
authors.lastname: Wilcox
authors.affiliation: Division of Nephrology and Hypertension, Hypertension, Kidney and Vascular Health Center, Georgetown University, Washington, DC, USA.
authors.forename: L
authors.initials: L
authors.lastname: Li
authors.affiliation: Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China.|Division of Nephrology and Hypertension, Hypertension, Kidney and Vascular Health Center, Georgetown University, Washington, DC, USA.
authors.forename: E Y
authors.initials: EY
authors.lastname: Lai
mesh_terms: D000818:Animals; D001160:Arterioles / Q000503:physiopathology*; D004195:Disease Models, Animal; D005919:Glomerular Filtration Rate; D007678:Kidney Glomerulus / Q000098:blood supply; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009392:Nephrectomy; D009929:Organ Size; D018384:Oxidative Stress / Q000502:physiology*; D051436:Renal Insufficiency, Chronic / Q000473:pathology / Q000503:physiopathology*; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*; D066253:Vascular Remodeling / Q000502:physiology*
chemical_list: D017673:Sodium Chloride, Dietary
keywords: efferent arteriole; myogenic response; reduced renal mass; vascular remodelling; wall compliance