Contribution of endothelin 1 to the vascular effects of diesel exhaust inhalation in humans

Jeremy P Langrish, Magnus Lundbäck, Nicholas L Mills, Neil R Johnston, David J Webb, Thomas Sandström, Anders Blomberg, David E Newby

Research output: Contribution to journalArticlepeer-review


Diesel exhaust inhalation impairs vascular function, and, although the underlying mechanism remains unclear, endothelin (ET) 1 and NO are potential mediators. The aim of this study was to identify whether diesel exhaust inhalation affects the vascular actions of ET-1 in humans. In a randomized, double-blind crossover study, 13 healthy male volunteers were exposed to either filtered air or dilute diesel exhaust (331±13 μg/m3). Plasma concentrations of ET-1 and big-ET-1 were determined at baseline and throughout the 24-hour study period. Bilateral forearm blood flow was measured 2 hours after the exposure during infusion of either ET-1 (5 pmol/min) or the ET(A) receptor antagonist, BQ-123 (10 nmol/min) alone and in combination with the ET(B) receptor antagonist, BQ-788 (1 nmol/min). Diesel exhaust exposure had no effect on plasma ET-1 and big-ET-1 concentrations (P>0.05 for both) or 24-hour mean blood pressure or heart rate (P>0.05 for all). ET-1 infusion increased plasma ET-1 concentrations by 58% (P0.05). Diesel exhaust inhalation increases vascular sensitivity to ET-1 and reduces vasodilatation to ET(A) receptor antagonism despite unchanged plasma ET-1 concentrations. Given the tonic interaction between the ET and NO systems, we conclude that diesel exhaust inhalation alters vascular reactivity to ET-1 probably through its effects on NO bioavailability.

Original languageEnglish
Pages (from-to)910-915
Number of pages6
Issue number4
Publication statusPublished - 1 Oct 2009


  • air pollution
  • particulate matter
  • endothelial function
  • endothelin receptor antagonists
  • ET-1
  • endothelin-1
  • blood pressure


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