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Evidence for the role of A 2B adenosine receptor in the regulation of vascular tone using A 2B KO mice
Author(s) -
Sanjani Maryam Sharifi,
Ponnoth Dovenia,
Roush Kevin,
Tilley Stephen,
Mustafa S. Jamal
Publication year - 2010
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.24.1_supplement.958.2
Subject(s) - agonist , adenosine , contraction (grammar) , medicine , chemistry , endocrinology , ccpa , receptor , adenosine receptor , adenosine a1 receptor , nucleoside , biology , biochemistry
Adenosine, an endogenous nucleoside, exerts its effects through its four receptor subtypes (AR): A 1 , A 2A , A 2B , and A 3 . Adenosine is involved in the regulation of vascular tone where its effects are subtype‐dependent. The contribution of ARs needs to be further investigated in order to better understand the heterogeneity of vasculature responses. In mice aorta, A 2A AR is known to be involved in vascular relaxation, however, the role of A 2B AR has not been studied in this tissue. To investigate this, we performed organ bath experiments. Tissues with <40% ACh relaxation to PE (10 −6 M) contraction were excluded (endothelial integrity). NECA, a non‐selective AR agonist, induced a significantly higher contraction in A 2B KO compared to WT (21.8±3.2% contraction vs 21.9±8.5% relaxation at 10 −5 M, p<0.01) showing that activation of A 2B AR may induce relaxation. CCPA, a selective A 1 agonist, induced contraction (38.9±6.3% at 10 −6 M) was significantly reduced in A 2B KO (5.9±7.8% at 10 −6 M, p<0.01) suggesting the down‐regulation of A 1 AR. Cl‐IBMECA, a selective A 3 agonist, showed significantly lower contraction in A 2B KO compared to WT (14.6±3.3% vs 42.9±5.3% at 10 −6 M, respectively) further suggesting the down‐regulation of A 3 AR in A 2B KO. These data show a relationship between A 2B and A 1 and A 3 ARs which must be taken into account in the control of vascular tone. Supported by HL027339, HL094447, HL071802, and T‐32 HL090610.