Aim Previous studies have demonstrated that ni- tric oxide (No) prostacyclin (PGI2) and ATP-sensi- tive K+ channel all participate in the regulation of hy- poxic cerebrovascular dilatation. but the interrelations of them still keep unclear. The aim of the study is to investigate the interrelations of these three vasodila- tive factors under hypoxia. Methods The experiments were Performed in new-born calf basilar arteral strips to observe the interrela-tions between NO and PGI:, Pt7[, and ATP-sensitive K+ channel, ATP-sensitive K channel and NO, re- spetively, in hypoxic cerebrovascular dilatation (the bypoxic Perfusion solation was prepared with PO2 6. 0 kPa, PCO2, 4. 7 kPa, and pH 7. 40±0. 02 ).Results The NO bad no effect of PGI2, but dilata-tion induced by NO appears to depend on production of PGI2, PGI2 had no obvious effect on ATP-sensitive K+ channel, but the effects of PGI2 may be dependent on openning of ATP-sensitive K - channel ; the effects of No may be not directely mediated by openning of ATP-sensitive K+ channel. and the activities of ATP- sensitive K+ channel seem isolated from effect of NO.Conclusions The response of hypoxic cerebrovas-cular dilatation are influenced obviously by No and PGI2 except reaction induced by ATP-sensitive K+ channel. There are some interrelative effects be-tween NO and PGI2, but the openning of ATP-sensi-tive K+ channel in not innuenced by them.