Adenosine A1 receptors and vascular reactivity

Authors:
Publisher website
Google Scholar
Abstract
Aim:  Blood pressure is higher in A1 receptor knock‐out (A1R−/−) mice than in wild type litter mates (A1R+/+) 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 A1 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 A1R−/− mice. However, in mesenteric arteries no contractile response was seen and adenosine‐mediated relaxation was identical between studied genotypes. A2B adenosine receptors, rather than A2A receptors, may be mainly responsible for the vasorelaxation induced by adenosine analogues in the examined mouse vessels. PP was higher in A1R−/− mice, but variability was unaltered. AIX was not different between genotypes, but the NECA‐induced fall was larger in A1R−/− mice.Conclusions:  The role of adenosine A1 receptors in regulating vessel tone differs between blood vessels. Furthermore, contractile effects on isolated vessels cannot explain the blood pressure in A1 knock‐out mice. The A1 receptor modulation of blood pressure is therefore mainly related to extravascular factors.

This publication has 28 references indexed in Scilit: