Premium
Inhibition or deletion of Adenosine A 2A receptor enhances acetylcholine‐induced vascular response: role of angiotensin‐II in A 2A AR ‐/‐ vs. C57Bl/6 mice
Author(s) -
Agba Stephanie O.,
Hanif Ahmad,
Ledent Catherine,
Stephen Tilley L.,
Nayeem Mohammed A.
Publication year - 2022
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2022.36.s1.l7712
Subject(s) - adenosine a2a receptor , acetylcholine , angiotensin ii , medicine , endocrinology , chemistry , adenosine , muscarinic acetylcholine receptor , receptor , biology , adenosine receptor , agonist
In previous studies, we showed that adenosine‐induced vascular relaxation was reduced in adenosine A 2A receptor (A 2A AR)‐null (A 2A AR ‐/‐ ) or A 2A AR‐inhibited C57Bl/6 mice. However, it is unknown the acetylcholine‐induced vascular response in A 2A AR ‐/‐ or A 2A AR‐inhibited C57Bl/6 mice; therefore, we hypothesized that the acetylcholine enhances endothelial‐dependent vascular relaxation in A 2A AR‐gene deleted (A 2A AR ‐/‐ ) or inhibited C57Bl/6 mice compared to their respective controls. Acetylcholine‐induced dose dependent vascular response was tested with SCH58261 (A 2A AR‐antagonist) in C57Bl/6 vs. non‐treated C57Bl/6 mice and angiotensin‐II (Ang‐II) in C57Bl/6 vs. non‐treated C57Bl/6 mice, Ang‐II treated A 2A AR ‐/‐ vs. non‐treated A 2A AR ‐/‐ mice and Ang‐II treated A 2A AR ‐/‐ vs. Ang‐II treated C57Bl/6 mice. In C57Bl/6 mice, SCH58261 (1µM) increased in acetylcholine‐induced dose‐dependent vascular relaxation compared to non‐treated C57Bl/6 mice. Similarly, in A 2A AR ‐/‐ mice, acetylcholine enhanced dose‐dependent vascular relaxation compared to C57Bl/6 mice. However, acetylcholine‐induced dose‐dependent vascular relaxation was reduced with angiotensin‐II (Ang‐II,1µM) in C57Bl/6 compared to non‐treated C57Bl/6 mice and acetylcholine‐induced dose‐dependent vascular relaxation was reduced with Ang‐II (1µM) in C57Bl/6 compared to A 2A AR ‐/‐ treated mice. Our data suggest that the acetylcholine dose‐dependent vascular relaxation is endothelial dependent and is enhanced in the absence or inhibition of A 2A AR unlike adenosine dose‐dependent vascular relaxation in mice.