Abstract

Ketanserin, when infused into the left thoracic vertebral artery of chloralose-anaesthetized cats, induced a significantly stronger hypotensive effect than when administered via the systemic circulation. The effect of ketanserin, which is initiated most likely in the pontomedullary region of the brain, proved to be dose dependent. The central hypotensive effect of ketanserin was accompanied by modest bradycardia, which was probably also of central nervous origin. The selective 5-HT2-receptor antagonist ritanserin, when infused into the left vertebral artery, did not lower blood pressure or heart rate, thus suggesting that central 5-HT2 receptors do not play a significant role in the initiation of ketanserin's central hypotensive action. Similarly, neither alpha 1- nor alpha 2-adrenoceptors in the central nervous system (CNS) appear to be involved in the hypotensive action of ketanserin, as concluded from pretreatment experiments with corynanthine and rauwolscine, respectively. The central hypotensive action could be blocked by atropine. This effect is located within the CNS but does not implicate a direct influence of ketanserin on CNS muscarinic receptors.

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