Angiotensin II stimulation alters vasomotor response to adenosine in mouse mesenteric artery: role for A1 and A2B adenosine receptors

• DOI: 10.1111/bph.13265
• Publication Date: 2015-07-31T02:22:53Z
• Authors: Vishal R Yadav; Mohammed A Nayeem; Stephen L Tilley; S Jamal Mustafa
• Keywords: Adenosine A1 receptor; Myograph

Background and Purpose Stimulation of the A 1 adenosine receptor angiotensin II type‐1 (AT receptor) causes vasoconstriction through activation cytochrome P450 4A (CYP4A) ERK1/2. Thus, we hypothesized that acute alters vasomotor response induced by non‐selective agonist, NECA, in mouse mesenteric arteries (MAs). Experimental Approach We used a Danish Myo Technology wire myograph to measure muscle tension isolated MAs from wild type (WT), 2B knockout (KO) mice. Western blots were performed determine expression AT receptors CYP4A. Key Results Acute exposure (15 min) attenuated NECA‐dependent vasodilatation enhanced vasoconstriction. This vasoconstrictor effect NECA‐treated was abolished KO mice WT treated with antagonist DPCPX, CYP4A inhibitor HET0016 ERK1/2 PD98059. In mice, on NECA‐induced shown be dependent receptors. Furthermore, increased II‐induced enhanced. addition, inhibition K ATP channels glibenclamide significantly reduced Conclusions Implications stimulation receptor‐dependent inhibited vasodilatation, leading net altered NECA MAs. interaction may important regulation BP.