Adenosine A 1 receptors and vascular reactivity

Aim: Blood pressure is higher in A 1 receptor knock‐out (A 1 R−/−) mice than in wild type litter mates (A 1 R+/+) and we have examined if this could be related to altered vascular functions. Methods: Contraction of aortic rings and mesenteric arteries were examined. To examine if the adenosine A 1 receptor‐mediated contraction of aortic muscle was functionally important we examined pulse pressure (PP) and augmentation index (AIX) using a sensor that allows measurements of rapid pressure transients. Results: Contraction of aortic rings to phenylephrine and relaxation to acetylcholine were similar between genotypes. The non‐selective adenosine receptor agonist N ‐ethyl carboxamido adenosine (NECA) enhanced the contractile response, and this was eliminated in aortas from A 1 R−/− mice. However, in mesenteric arteries no contractile response was seen and adenosine‐mediated relaxation was identical between studied genotypes. A 2B adenosine receptors, rather than A 2A receptors, may be mainly responsible for the vasorelaxation induced by adenosine analogues in the examined mouse vessels. PP was higher in A 1 R−/− mice, but variability was unaltered. AIX was not different between genotypes, but the NECA‐induced fall was larger in A 1 R−/− mice. Conclusions: The role of adenosine A 1 receptors in regulating vessel tone differs between blood vessels. Furthermore, contractile effects on isolated vessels cannot explain the blood pressure in A 1 knock‐out mice. The A 1 receptor modulation of blood pressure is therefore mainly related to extravascular factors.