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reported that the highest level of specific HlGReSdSO binding was found in homogenates of the area postrema and the vagus nerve. Direct injection of the 5 HT3 receptor antagonist into the region postrema briefly inhibits cisplatin Aurora B inhibitor induced emesis in ferrets. These findings recommend a role for central 5 HT3 receptors inside the mechanisms underlying the emesis induced by anticancer agents but will not rule out a peripheral website of action. As a result, emesis might be evoked by activation of 5 HT3 receptors positioned on afferent nerve pathways foremost in the viscera to the region postrema. Y 25130 was a potent inhibitor in the Von Bezold Jarisch effect induced by 5 HT. This suggests that Y 25130 blocks sensory input in the web-sites of sensory nerve endings and/or the sensory nerve itself.

Neither of these effects of DOI could be blocked by prior administration of ketanserin, a S HTj antagonist, the 5 HT,c/5HT2 antagonist ritanserin, or the putative S HT,a antagonist, pindolol. Ketanserin has been shown to significantly attenuate the wet dog shake behaviour induced by administration of 5 hydroxytryptophan and DOM induced alterations in locomotive behaviour were also blocked by ketanserin. Thus the doses of ketanserin used in this study would antagonise 5 HT2 receptors. Ritanserin can antagonise 1 5 hydroxytryptophan induced flat body posture, and at a higher dose blocks other 1 5 HTP induced behaviours, and this blockade correlates with the in vitro affinity of ritanserin for S HTj and 5 HTjc receptors. These results BI-1356 indicate that at the dose used in the present study ritanserin will antagonise both 5 HT,c and S HTj receptors.

This similarity in the doses of S HTj receptor antagonists required for antiplatelet and antiarrhythmic activity reinforces our hypothesis that the antiarrhythmic activity of these drugs depends on their ability to reduce platelet aggregation. In contrast, the inability of methiothepin to reduce reperfusion induced PARP arrhythmias despite its antiplatelet effect appears to contradict the above hypothesis. However, only ADP induced aggregation and the ability of 5 HT to enhance this were measured in the present experiments. It is possible that methiothepin may have some other action which promotes platelet aggregation mediated via other agents. For example, we have some evidence that methiothepin potentiates responses mediated via stimulation of 02adrenoceptors. In anaesthetized rats, methiothepin caused dose dependent increases in pressor PARP responses to low doses of noradrenaline.