Adenosine elicits vasodilatation in perfused efferent arterioles of the mouse

Abstract

Adenosine induces vasoconstriction of the mouse renal afferent arteriole via A1 adenosine receptors however the effect of adenosine on the efferent arteriole is unclear. We therefore used the isolated perfused cortical efferent arterioles from mouse kidneys to determine the response to adenosine and the type of adenosine receptors. Efferent arterioles were identified by their location and size compared to the afferent arteriole of the same glomerulus. Adenosine (Ado) applied to the bath in the concentration range between 10−9 and 10−4 M (three minutes at each concentration) had no effect on the efferent arteriole whereas high potassium (100 mM) elicited full constriction from 4.8 +/− 0.6 μm to 0.0 +/− 0.0 μm. However after preconstriction of the vessels with the tromboxane analogue U46619 adenosine dose dependently dilated the efferent arteriole (mean diameter: U46619 10−7 M 0.0 +/− 0.0 μm, U46619 + ado 10−8 M 0.0 +/− 0.0 μm, U46619 + ado 10−6 M 1.7 +/− 0.6 μm, U46619 + ado 10−4 M 4.3 +/− 0.6 μm) suggesting involvement of A2b adenosine receptors. This adenosine induced vasodilatation was inhibited by 15 minutes pretreatment with the A2 adenosine receptor antagonist DMPX (10−4 M). Using RT-PCR with primers specific for the two types of A2 adenosine receptors, A2a and A2b we found expression of both A2a and A2b adenosine receptors in microdissected efferent arterioles. We conclude that adenosine leads to vasodilatation in the efferent arteriole of mouse through an activation of A2 adenosine receptors presumably A2b. Sources of research support were the Danish Medical Research Council and the Danish Heart Foundation.