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In helical strips of dog cerebral, coronary, mesenteric, renal, and femoral arteries, the addition of thiamylal and thiopental, 10−5 to 10−5M, caused a dose-related contraction; the contraction was significantly more intense in cerebral than in extracerebral arteries. Secobarbital caused a slight contaction only in the cerebral artery. In contrast, pentobarbital did not produce a contraction in any artery studied. The thiamylal-induced contraction was not affected by treatment with phentolamine, diphenhydramine, or cinanserin but was attenuated by treatment with Ca entry blockers, such as nifedipine or diltiazem. In the cerebral artery soaked in Ca++-free media for 60 min, the addition of Ca++ produced triphasic responses; a transient contraction followed by a relaxation and a slowly developing, persistent contraction. The persistent contraction was potentiated by 10−4M thiamylal but abolished at 10−3M. In the mesenteric artery soaked in Ca++-free media, the addition of Ca++ produced only a slight contraction, which was potentiated by thiamylal (10−4 and 10−4 M). It is concluded that thiobarbiturates are more potent vasoconstrictors than oxybarbiturates and that the barbiturates produce greater contraction in cerebral arteries than in extracerebral arteries. The thiamylal-induced contraction appears to be associated mainly with influx of Ca++ from extracellular fluids.