Histamine and 2,2-pyridylethylamine, an H1-receptor agonist, (both 10(-8)-10(-3) M) caused contraction of human cerebral artery preparations in the absence of active tension, while dimaprit, an H2-receptor agonist, caused vasorelaxation. The histamine-induced vasoconstriction was blocked non-competitively by tripelennamine, an H1-receptor antagonist. In the presence of cimetidine, an H2-receptor antagonist, histamine-induced contraction was enhanced. The histamine-induced contraction was not affected by phentolamine or propranolol, but abolished by nifedipine. In prostaglandin F2 alpha-precontracted arteries, histamine and dimaprit caused relaxation, while 2,2-pyridylethylamine had no apparent effect. Histamine-induced relaxation was much greater in the presence than in the absence of an H1-antagonist. The vasorelaxation induced by histamine in the presence of an H1-antagonist was also inhibited by an H2-antagonist. Histamine caused no apparent relaxation in precontracted preparations without endothelium. The present results provide further evidence that histamine causes either vasocontraction or vasodilation in human cerebral arteries, and suggest that vasocontraction and vasorelaxation are due to the activation of H1- and H2-receptors, respectively. The relaxation induced by histamine may also be related to the endothelium-derived relaxing factors released from endothelial cells.

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