Summary Intravenous histamine caused a dose‐dependent fall in mean arterial pressure, often preceded by a brief rise. After burimamide the initial pressor response was potentiated and the depressor response was abolished or reversed; in contrast, niepyramine abolished the pressor response and potentiated the hypotensive phase. After both drugs in combination the response to histamine was abolished. It is concluded that the response to histamine is a balance between a pressor effect mediated by mrpyramine‐sensitive H 1 receptors, and a depressor effect mediated by burimamide‐sensitive H 2 receptors.
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Carroll et al. (1974) studied this question.