Endothelium-dependent relaxations to adenosine in juvenile rabbit pulmonary arteries and veins

Robin H Steinhorn, F. C. Morin, D. G L Van Wylen, S. F. Gugino, E. C. Giese, J. A. Russell

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


We studied the actions of adenosine and its analogues 5'-(N- ethylcarboxamido)-adenosine (NECA) and N6-cyclohexyladenosine (CHA) in pulmonary vessels isolated from juvenile rabbits. Pulmonary arteries relaxed in a concentration-dependent fashion to all three compounds. Pretreatment with the methylxanthine 8-p-sulfophenyltheophylline shifted the concentration-response curves to adenosine and NECA rightward, indicating that the vasodilator effects were mediated by the adenosine receptor. The order of potency of adenosine compounds was NECA > adenosine > CHA, indicating that the A2-receptor mediates relaxations to adenosine in rabbit pulmonary arteries. Endothelium rubbing attenuated relaxations to adenosine at concentrations of ≤3 x 10-7 M and to all NECA concentrations. Inhibition of nitric oxide synthase with N(G)-nitro-L-arginine (L-NNA) similarly attenuated relaxations at concentrations of ≤3 x 10-7 M for adenosine and ≤3 x 10-8 M for NECA. With the use of the same methods, a substantial endothelial contribution was additionally observed in pulmonary veins to the vasodilator effects of NECA. We conclude that adenosine, and the more specific A2-receptor agonist NECA, dilate pulmonary arteries and veins isolated from young rabbits via a mechanism that is partially dependent on endothelium-derived nitric oxide.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number5 35-5
StatePublished - 1994
Externally publishedYes


  • endothelium-dependent relaxing factor
  • nitric oxide
  • vascular smooth muscle
  • vasodilation

ASJC Scopus subject areas

  • Physiology
  • Agricultural and Biological Sciences(all)


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