The effects of vasopressin on the cerebral circulation were studied in conscious goats and in isolated human and goat cerebral arteries. Infusion of 1 to 12 mU of vasopressin into the internal maxillary artery of unanesthetized goats caused dose-dependent reductions in cerebral blood flow, a decrease of 36 +/- 4.7% (mean +/- S.E.) occurring with the highest dose. Cumulative application of vasopressin (10(-12) to 10(-6) M) markedly constricted human and goat cerebral arteries in vitro, the effect being more prominent in human vessels. (1-Deaminopenicillamine, 4-valine)-8-D-arginine-vasopressin, a competitive antagonist of the pressor effects of vasopressin, partially inhibited the cerebral vasoconstriction produced by vasopressin in vivo and in vitro without affecting the vasoconstrictor responses to norepinephrine, 5-hydroxytryptamine and potassium chloride. The results indicate that low concentrations of vasopressin produce constriction of cerebral vessels by direct excitatory effects on specific receptor sites. This effect should be considered in certain pathophysiological states in which vasopressin is released in amounts that could interfere with the proper blood supply to the brain.

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