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In helical strips of dog cerebral arteries exposed to Ca 2+ -free medium under hypoxic conditions (95% N 2  and 5% CO 2 ), prostaglandin (PG) F 2α  produced a slight tonic contraction. The addition of Ca 2+  evoked a phasic contraction followed by relaxation and a sustained contraction, and reoxygenation elicited an additional tonic contraction of moderate magnitude. When the PGF 2α -induced contraction was stabilized in Ca 2+ -free medium, reoxygenation contracted the arteries only slightly. Treatment with the stable PGI 2  analogues PGI 2  methylester and TRK-100 attenuated the contractions caused by PGF 2α  and Ca 2+  and abolished almost completely the reoxygenation-induced contraction. Treatment with nitroglycerin inhibited the contractions caused by PGF 2α  and Ca 2+ , but did not significantly alter the contraction induced by reoxygenation. The Ca 2+  entry blockers diltiazem, flunarizine, and felodipine did not alter the PGF 2α -induced contractions, but attenuated the contractions caused by Ca 2+  and reoxygenation. The vasodilator agents used appear to interfere differently with the release of Ca 2+  from intracellularly stored sites and the transmembrane Ca 2+  influx through receptor-operated channels under hypoxia and normoxia. The cerebroarterial contraction caused by reoxygenation may be associated mainly with increased Ca 2+  influx from receptor activation and tissue oxygenation, which is markedly suppressed by PGI 2  analogues and moderately attenuated by Ca 2+  entry blockers but not significantly influenced by nitroglycerin.

Reoxygenation and Calcium-Induced Cerebroarterial Contractions as Affected by Vasodilator Agents