Mechanism of circulatory effects of chlorcyclizine

Abstract Intravenous administration of chlorcyclizine produced a biphasic response characterized by an initial and abrupt depressor response followed by a gradual and sustained pressor response. Analysis of this response showed that the initial depressor response was of peripheral origin and was not mediated by cholinergic, histaminergic or serotonergic mechanisms, whereas the delayed pressor response apparently resulted from activation of supramedullary sympathetic neurones leading to a massive release of catecholamines from the sympatho-adrenal system.