The purinergic branchial vasomotor control in rainbow trout (Oncorhynchus mykiss) was studied using an epi-illumination microscope equipped with a water-immersion objective. Cardiac output (Q), heart rate, and dorsal (PDA) and ventral (PVA) aortic pressures were recorded simultaneously. Prebranchial injection of adenosine or the A1-receptor agonist N6-cyclopentyl-adenosine (CPA) constricted the distal portion of the filament vasculature, which coincided with an increase of PVA. The A2-receptor agonist PD-125944 was without effect. After adenosine and CPA injection, an overflow of blood to the secondary system was repeatedly observed unless blood flow came to a complete stop. The lack of a concomitant reduction of Q suggested a redistribution of blood to the secondary system and to more proximal parts of the filament. The branchial effects of adenosine and CPA were completely blocked by the unspecific adenosine receptor antagonist amino-phylline and the specific A1-receptor antagonist N6-cyclopen-tyltheophylline. The results suggest that A1-receptors alone mediate the branchial vasoconstriction observed. Thus the responses of the branchial vasculature to adenosine include a vasoconstriction of the filament vasculature mediated via specific A1 receptors and a redistribution of blood flow to the secondary system and to proximal parts of the filament. Additional cardiovascular effects of adenosine included decreased systemic vascular resistance and heart rate.