Selective COX-2 inhibitors and renal injury in salt-sensitive hypertension

Hypertension. 2005 Feb;45(2):193-7. doi: 10.1161/01.HYP.0000153053.82032.bf. Epub 2005 Jan 3.

Abstract

In view of the ongoing controversy of cardiorenal safety of selective COX-2 inhibitors (coxibs), the present study was designed to examine the effects of 2 different coxibs, celecoxib and rofecoxib, compared with a traditional NSAID, diclofenac, and placebo on renal morphology and function in salt-sensitive hypertension. Salt-sensitive (DS) and salt-resistant (DR) Dahl rats were fed with NaCl-enriched diet (4% NaCl) for 8 weeks. Diclofenac (DS-diclofenac), rofecoxib (DS-rofecoxib), celecoxib (DS-celecoxib), or placebo was added to chow from weeks 6 to 8. Immunostaining for monocytes/macrophages (ED1) and cytotoxic T lymphocytes (CD8) was performed. In addition, renal morphology and proteinuria were assessed. Renal cortex mRNA was isolated for determination of COX-2, eNOS, and CRP mRNA by real-time reverse-transcriptase polymerase chain reaction. Untreated hypertensive animals showed glomerular injury including collapsing glomerulopathy, mesangial sclerosis, mesangiolysis, extracapillary proliferation, protein drops, and an especially high grade of glomerulosclerosis (P<0.05 versus DR-placebo) and CD8-positive and ED1-positive cells (P<0.01 versus DR-placebo), which was improved by celecoxib but not by diclofenac and rofecoxib. C-reactive protein mRNA in renal cortex was increased in DS-placebo animals (P<0.05 versus DR-placebo) and normalized by celecoxib (P<0.05 versus DS-placebo), whereas eNOS mRNA was decreased in the DS-rofecoxib group (P<0.05 versus DR-placebo, DS-celecoxib, and DS-diclofenac). Proteinuria was observed in hypertensive animals (P<0.0001 versus DR-placebo), increased by rofecoxib (P<0.05 versus DS-placebo), and normalized by celecoxib (P=0.0015 versus DS-placebo). This head-to-head comparison of selective and nonselective COX inhibitors demonstrates differential effects of coxibs on renal morphology and function in salt-dependent hypertension.

MeSH terms

  • Animals
  • Blood Pressure / drug effects
  • Blood Vessels / pathology
  • C-Reactive Protein / genetics
  • CD8-Positive T-Lymphocytes / pathology
  • Celecoxib
  • Cell Count
  • Cyclooxygenase 2
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors / pharmacology*
  • Diclofenac / pharmacology
  • Hemodynamics / drug effects
  • Hypertension / chemically induced*
  • Hypertension / metabolism
  • Hypertension / pathology*
  • Hypertension / physiopathology
  • Immunohistochemistry
  • Kidney / blood supply
  • Kidney / metabolism
  • Kidney / pathology*
  • Kidney / physiopathology
  • Kidney Cortex / metabolism
  • Kidney Glomerulus / pathology
  • Lactones / pharmacology
  • Monocytes / pathology
  • Nitric Oxide Synthase / genetics
  • Nitric Oxide Synthase Type III
  • Prostaglandin-Endoperoxide Synthases / metabolism
  • Pyrazoles / pharmacology
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Inbred Dahl
  • Sodium Chloride*
  • Sulfonamides / pharmacology
  • Sulfones / pharmacology

Substances

  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors
  • Lactones
  • Pyrazoles
  • RNA, Messenger
  • Sulfonamides
  • Sulfones
  • rofecoxib
  • Diclofenac
  • Sodium Chloride
  • C-Reactive Protein
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type III
  • Nos3 protein, rat
  • Cyclooxygenase 2
  • Prostaglandin-Endoperoxide Synthases
  • Celecoxib