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Flunarizine relaxed isolated canine arteries precontracted with prostaglandin (PG) F2 alpha, epithio-methano-thromboxane A2 and K+; the relaxation was in the order of cerebral greater than renal greater than mesenteric = coronary arteries, when contracted with PGF2 alpha or the thromboxane A2 analogue. Flunarizine-induced relaxation was unaffected by treatment with atropine, propranolol, cimetidine, cimetidine, chlorpheniramine, aminophylline and indomethacin, and by removal of endothelium. Under normoxia, flunarizine attenuated contractions elicited by Ca2+ in the K+-stimulated cerebral and mesenteric arteries that had been previously exposed to Ca2+-free media to a greater extent than that in PGF 2 alpha-stimulated preparations. The Ca2+-induced contraction in cerebral arteries was more sensitive to flunarizine than that in mesenteric arteries. Contractions caused by PGF2 alpha in Ca2+-free media were not influenced by flunarizine. In cerebral and mesenteric arteries that had been previously exposed to Ca2+-free media and severe hypoxia and then stimulated by PGF2 alpha and Ca2+, reoxygenation produced a persistent contraction. Flunarizine suppressed the reoxygenation induced-contraction. It is concluded that flunarizine dilates cerebral arteries predominantly over the other arteries; the vasodilatation appears to derive from an interference with the transmembrane Ca2+ influx that occurs through a voltage-dependent process and, to a lesser extent, receptor-operated channels, but not with the Ca2+ release from stored sites. Contraction induced by reoxygenation is expected to be due mainly to the transmembrane influx of Ca2+, which is also suppressed by flunarizine.

Vasodilator actions of flunarizine in isolated dog cerebral and extracerebral arteries.