Cellular Calcium and the Contraction Induced by Prostaglandin F2α in Feline Cerebral Arteries

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Abstract
The influences of different calcium‐entry blockers, sialidase and caffeine on the biphasic contraction induced by prostaglandin (PG) F2α in the feline basilar artery (BA) were studied in calcium‐free medium. After incubation in calcium‐free solution, PGF2α induced a contraction of the BA amounting to 87% of the contraction in calcium‐containing solution. The response was biphasic in 41 out of 42 vessel segments. PGF2α‐induced contractions were markedly attenuated in TRIS‐buffered solutions as compared to contractions in Krebs solution. PGF2α failed to induce a biphasic contraction (8 out of 9 preparations) in calcium‐free HEPES‐buffered solution. Calcium entry blockade with 1 mM manganese or 10−5M diltiazem abolished the second and major phase of the PGF2α‐induced contraction in calcium‐free Krebs solution. The second contraction phase was also eliminated in four out of five preparations pretreated with sialidase (1 unit/ml for 30 min.), but was unaffected by a brief exposure to 20 mM caffeine in calcium‐free medium. The present findings strongly support previous suggestions that a major part of the PGF2α‐induced contraction in calcium‐free medium is mediated via the release of calcium bound to the exterior aspect of the cell membrane.