Effects of prostanoids on isolated feline cerebral arteries

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Abstract
The roles of extra- and intracellular Ca for the contractile effects of PGF2.alpha. [prostaglandin] in the feline basilar artery (BA) were investigated. Comparisons were made with contractions induced by K+ and noradrenaline (NA, [norepinephrine]). Addition of nifedipine to PGF2.alpha.- or K+ (124 mM)-contracted arteries resulted in an incomplete relaxation, whereas NA-contracted vessels were completely relaxed. Incubation of the preparations in a Ca-free medium containing 10-5 M EGTA [ethyleneglycol-dis(.beta.-aminoethylether)-N,N,N'',N''-tetraacetic acid] for 5-10 min almost abolished contractions induced by K+ and NA. In contrast, 63% of the response to PGF2.alpha. remained after pretreatment of the arteries in a Ca-free solution for 40 min; PGF2.alpha. produced a biphasic contraction in 17 out of 20 preparations consisting of a rapidly developing initial phase followed by a 2nd increase in tension after 1-6 min. The 2nd 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 Ca-free medium for 40-120 min and K+-depolarization, re-addition of Ca elicited contractions at lower concentrations in the presence of PGF2.alpha. than in controls. PGF2.alpha.-induced contractions in the feline BA are evidently considerably less dependent on extracellular Ca than contractions evoked by K+ or NA. PGF2.alpha. appears to be able to release Ca from 2 cellular stores and may also promote Ca influx through the cell membrane.