Pressure is proinflammatory in lung venular capillaries

J Clin Invest. 1999 Aug;104(4):495-502. doi: 10.1172/JCI6872.


Endothelial responses may contribute importantly to the pathology of high vascular pressure. In lung venular capillaries, we determined endothelial [Ca(2+)](i) by the fura-2 ratioing method and fusion pore formation by quantifying the fluorescence of FM1-43. Pressure elevation increased endothelial [Ca(2+)](i). Concomitantly evoked exocytotic events were evident in a novel spatial-temporal pattern of fusion pore formation. Fusion pores formed predominantly at vascular branch points and colocalized with the expression of P-selectin. Blockade of mechanogated Ca(2+) channels inhibited these responses, identifying entry of external Ca(2+) as the critical triggering mechanism. These endothelial responses point to a proinflammatory effect of high vascular pressure that may be relevant in the pathogenesis of pressure-induced lung disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Blood Pressure / physiology*
  • Calcium / metabolism
  • Capillaries / physiology
  • Endothelium, Vascular / physiology
  • Inflammation / etiology*
  • Inflammation / physiopathology
  • Lung / blood supply*
  • Lung / physiopathology
  • Lung Injury
  • Microscopy, Fluorescence
  • P-Selectin / metabolism
  • Pulmonary Circulation / physiology
  • Rats
  • Rats, Sprague-Dawley


  • P-Selectin
  • Calcium