1 An investigation was carried out to determine whether the centrally acting hypotensive drugs whose mechanisms of action are due either to activation of 5-HTIA receptors (flesinoxan, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and urapidil also an a,-adrenoceptor antagonist) or to activation of M2-adrenoceptors (clonidine and moxonidine) cause differential sympathoinhibition. 2 Cats were anaesthetized with a-chloralose and simultaneous recordings were made of whole cardiac, splanchnic and renal nerve activity, blood pressure and heart rate. Cumulative doseresponse (i.v.) curves were constructed in separate experiments for the above hypotensive agents on these parameters. 3 Renal nerve activity was found to be more sensitive to the sympathoinhibitory action of flesinoxan and 8-OH-DPAT when compared with cardiac nerve activity, whereas the reverse was observed for clonidine and moxonidine, cardiac being more sensitive than renal nerve activity. Splanchnic nerve activity was similarly affected by all drugs. Furthermore at the highest dose, all drugs tended to cause complete inhibition in all regional sympathetic nerve outflows. 4 Urapidil differed from all the above hypotensive drugs in that it caused a similar degree of sympathoinhibition in all sympathetic outflows at all doses. It is suggested that this may be due to the ability of urapidil to block central a,-adrenoceptors in addition to stimulation of 5-HTlA receptors. IntroductionThere is a large amount of evidence to suggest that 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and flesinoxan activate 5-HTlA receptors to cause their hypotensive action McCall et al., 1987;Ramage & Fozard, 1987;Doods et al., 1988;Wouters et al., 1988;Laubie et al., 1989) and that such an action is entirely within the central nervous system. However, only moderate thoracic preganglionic sympathoinhibition is observed in anaesthetized cats (Ramage & Fozard, 1987;Ramage et al., 1988). One explanation for this lack of correlation between the thoracic sympathoinhibitory action and the hypotensive action of 8-OH-DPAT and flesinoxan is that these drugs could be having a more potent sympathoinhibitory action at a different level or levels of sympathetic outflow. In this respect the sympathoinhibitory action of flesinoxan on renal ' Author for correspondence.outflow, when compared with other sympathetic outflows has been shown to be greater (Ramage et al., 1988). However a weakness of this latter investigation was that the recordings made from different sympathetic outflows were carried out in separate animals and further, that some of the outflows were recorded from preganglionic, while others were recorded from postganglionic nerves. In order to overcome these weaknesses the present experiments were carried out in which the sympathoinhibitory actions of flesinoxan and 8-OH-DPAT were studied on cardiac, splanchnic and renal nerve activity recorded simultaneously in the same animal. Further, the effects of other hypotensive agents, urapidil (which has also been shown to bind...

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Specimens with a bone mineral density in the range of 0.263-0.997 g/cm2 failed at a mean load of 339 N when the load was applied through the spinous process hook of a flexible fixation device.