Effects of prostanoids on isolated feline cerebral arteries

The roles of extra-and intracellular calcium for the contractile effects of PGF_2α in the feline basilar artery (BA) were investigated. Comparisons were made with contractions induced by K⁺ and noradrenaline (NA). Addition of nifedipine to PGF_2α-or K⁺ (124 mM)-contracted arteries resulted in an incomplete relaxation, whereas NA-contracted vessels were completely relaxed. Incubation of the preparations in a calcium-free medium containing 10^-5 M EGTA for 5–10 min almost abolished contractions induced by K⁺ and NA. In contrast, 63 % of the response to PGF_2α remained after pretreatment of the arteries in a calcium-free solution for 40 min; PGF_2α produced a biphasic contraction in 17 out of 20 preparations consisting of a rapidly developing initial phase followed by a second increase in tension after 1–6 min. The second phase was absent if the EGTA-concentration was increased to 10^-4 M, or if the arteries were pre-treated with nifedipine. After incubation of the arteries in a calcium-free medium for 40–120 min and K⁺-depolarization, re-addition of calcium elicited contractions at lower concentrations in the presence of PGF_2α than in controls. The results suggest that PGF_2α-induced contractions in the feline BA are considerably less dependent on extracellular calcium than contractions evoked by K⁺ or NA. PGF_2α appears to be able to release calcium from two cellular stores, and may also promote calcium influx through the cell membrane.