Infection by the malaria parasite induces organic osmolyte and anion channels of the host erythrocyte which mediate the regulatory volume decrease of the host cell. The effect of purinoceptor agonist/antagonists on the osmolyte channels and on the intraerythocytic parasite amplification was assessed by whole-cell patch clamp recording, colloid osmotic hemolysis in isosmotic sorbitol solution, and flow cytometry using the DNA/RNA-specific dye Syto16. As a result, the purinoceptor antagonists suramin (50 mM) and MRS2179 (10-100 mM) significantly inhibited while extracellular ATP (100 mM) increased the appearance of the osmolyte channels in P. falciparum-infected human erythrocytes. Similarly, suramin injected intraperitonally (500 mg / kg B.W.) into P. berghei-infected mice decreased the appearance of the osmolyte channel. Moreover, suramin inhibited in vitro amplification and DNA/RNA synthesis of P. falciparum and in vivo growth of P. berghei. Following infection of mice with P. berghei osmolyte channel activity was significantly less in infected erythrocytes from P2y1-/- mice than in those from wildtype mice, a finding suggesting the involvement of P2y1 purinoceptor subtypes. In accordance with the functional data immunoblotting revealed the expression of P2y1 protein in human erythrocytes. In conclusion, induction of the osmolyte permeability in Plasmodium-infected erythrocytes depends on autocrine P2y1 purinoceptor signalling.