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Attenuation of adenosine receptor‐mediated vasorelaxation by L‐NAME in mouse aorta
Author(s) -
Ansari Habib R.,
Nadeem A.,
Talukder M. A.H.,
Mustafa S. Jamal
Publication year - 2006
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.20.5.lb17-a
Subject(s) - adenosine , adenosine receptor , endothelium , chemistry , aorta , cgs 21680 , medicine , endocrinology , vasodilation , receptor , pharmacology , biology , biochemistry , agonist
In BALB/c mouse thoracic aorta with intact endothelium, adenosine and its analogs produce a dose‐response (DR) relaxation with a rank order of potency favoring A 2B (NECA>CAD>adenosine>> CGS 21680; Talukder et al. LB4, FASEB J. 13(3), 1999). This was further supported by the fact that the A 2B ‐receptor antagonist, alloxazine shifted DR to right for NECA. However, this study did not investigate the role of endothelium in adenosine‐mediated relaxation of mouse aorta. Thus, the present study was conducted to investigate the role of endothelium in adenosine receptor‐mediated relaxation. In organ bath studies, in intact endothelium, the EC 50s for NECA, CAD and adenosine were found to be 0.05, 1.3 and 3.1 x 10 −4 M, respectively. However, in the absence of endothelium, the EC 50s for NECA, CAD and adenosine were; 0.098, 1.5 and 0.12 x 10 −4 M, respectively indicating a shift in DR to the right. The intactness of endothelium in aortic tissue was tested with acetylcholine. NECA‐induced DR relaxation was significantly blocked by L‐NAME (10 −4 M) in endothelium‐intact tissues; whereas no inhibition was found in endothelium‐denuded tissues. Moreover, the involvement of NO was confirmed by measuring total nitrites and nitrates (NOx) in endothelium‐intact and ‐denuded aorta. NOx levels with L‐NAME (10 −4 M) alone and in combination with L‐arginine (10 −4 M) were 59% and 96%, respectively with respect to control (NECA+PE, p<0.05). These data demonstrate that adenosine‐receptor mediated relaxation in mouse aorta is partially dependent on endothelium through adenosine A 2B ‐receptor. (Supported by HL 027339)