Shear stress and the endothelium

B. J. Ballermann*, A. Dardik, E. Eng, A. Liu

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

293 Scopus citations


Vascular endothelial cells (ECs) in vivo are influenced by two distinct hemodynamic forces: cyclical strain due to vessel wall distention by transmural pressure, and shear stress, the frictional force generated by blood flow. Shear stress acts at the apical cell surface to deform cells in the direction of blood flow; wall distention tends to deform cells in all directions. The shear stress response differs, at least partly, from the cyclical strain response, suggesting that cytoskeletal strain alone cannot explain it. Acute shear stress in vitro elicits rapid cytoskeletal remodeling and activates signaling cascades in ECs, with the consequent acute release of nitric oxide and prostacyclin; activation of transcription factors nuclear factor (NF)κB, c-fos, c-jun and SP-1; and transcriptional activation of genes, including ICAM-1, MCP-1, tissue factor, platelet-derived growth factor-B (PDGF-B), transforming growth factor (TGF)-β1, cyclooxygenase-II, and endothelial nitric oxide synthase (eNOS). This response thus shares similarities with EC responses to inflammatory cytokines. In contrast, ECs adapt to chronic shear stress by structural remodeling and flattening to minimize shear stress. Such cells become very adherent to their substratum and show evidence of differentiation. Increased adhesion following chronic shear stress has been exploited to generate vascular grafts with confluent EC monolayers, retained after implantation in vivo, thus overcoming a major obstacle to endothelialization of vascular prostheses.

Original languageEnglish (US)
Pages (from-to)S100-S108
JournalKidney International, Supplement
Issue number67
StatePublished - 1998


  • Ca
  • Diacylglycerol
  • Differentiation
  • Intimal hyperplasia
  • Mechanical-chemical coupling
  • Mitogen-activated protein kinase
  • Nitric oxide
  • Nuclear factor κ B
  • Phospholipase C
  • Platelet- derived growth factor B
  • Protein kinase C
  • Strain
  • Stress-activated protein kinase
  • Transcription factors
  • Vascular prosthesis

ASJC Scopus subject areas

  • Nephrology


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