The aim was to characterize Ado effects via A1- and A2-receptors and the interaction with Angiotensin II (Ang II) in afferent arterioles. The effect of Ado, Ado-receptor agonists, and antagonists were investigated in isolated, perfused afferent arterioles (Af) of mice. Ado constricted Af in concentrations of 10–10 to 10–7 mol/l (-7%) and dilated it to control values in concentrations of 10–6 to 10–4 mol/l. This biphasic course was transformed into a dose dependent constriction in presence of Ang II (10–10 mol/l). The A1-agonist CPA (10–7 mol/l) constricted Af (-7%). CPT (10–5 mol/l, A1-antagonist) inhibited the constriction response to Ado. The A2A-agonist CGS 21680 (10–7 mol/l) also dilated the Af (12%). A1(-/-) mice did not show a contractile phase in the Ado-concentration-response. Inosine (10–11 to 10–5 mol/l), which activates A3-receptors, did not change arteriolar diameters. Ado 10–8 mol/l increased the Ang II-response of Af, while Ado 10–5 mol/l did not. Our results indicate the contribution of A1- and A2-receptors in the control of Af. The dramatic change in the Ado-response by Ang II and the potentiation of the Ang II-response by Ado (10–8 mol/l) point at the importance of the Ado-Ang II interaction in this context.