Adenosine is an end-product of purinergic metabolism and is produced excessively in the tissues exposed to hypoxia/ischemia. In these tissues, such produced adenosine induces profound vasodilation, which represents a counter regulatory mechanism against hypoxia. In the present study, we analysed the effect of adenosine on angiotensin II-induced contraction in the mesenteric vascular bed. Repeated exposure of the mesenteric artery to angiotensin II (Ang II) caused rapid desensitisation of the contraction to about 30% of the control value. Incubation of the vessels with adenosine re-established the contractile response to approx. 90% of the control contraction. Inhibition of adenosine receptors did not affect the re-sensitisation, whereas inhibition of the nucleotide transport abolished the effect of adenosine. The phosphorylation of the regulatory myosin light chain was significantly increased in the arteries incubated with adenosine as compared to untreated controls. In conclusion, adenosine causes re-sensitisation of the Ang II contraction in mesenteric arteries by an intracellular action, which includes phosphorylation of myosin light chain and thus increasing calcium sensitivity.