The contractile and relaxant effects of various prostanoids were studied on isolated human pial arteries. Contractions were elicited with the following order of potency: U46619≅U44069>PGB2>PGF2a>PGE2≅PGD2>PGF1a≥TXB2, indicating that prostanoid‐induced contractions probably are mediated by a thromboxane‐sensitive receptor. Relaxation of PGF2a‐contracted arteries was induced with the order of potency: PGE2>PGE1>PGD2≅PGD1. Vessels contrated by K+were relaxed only by PGE,. Since PGI2was previously found to be more potent than all the prostanoids tested in the present study, relaxant responses are probably mediated via a PGI2‐sensitive receptor. The roles of free extracellular and cellularly bound calcium for the contractile effects of PGF2aand K+were estimated by incubating the arteries for various times in calcium‐free medium containing 10‐5M EGTA. Incubation for 5–10 min abolished K+‐induced contractions, whereas after 40 min of incubation PGF2astill induced contractions that reached 70% of control. The PGF2a‐induced contraction was biphasic in 8 out of 10 preparations. The second phase could be eliminated by increasing the EGTA‐concentration to 10‐4M, as well as by nifedipine pretreatment. In calcium‐free, high K+medium calcium‐induced contractions were elicited at lower concentrations in the presence of PGF2a. The results suggest that PGF2a‐induced contractions in human pial arteries are relatively independent of free extracellular calcium. PGF2amay promote trans‐membrane influx of calcium, as well as release calcium from seemingly