THE EFFECTS OF INTRACISTERNAL ADMINISTRATION OF α‐ADRENORECEPTOR AGONISTS ON THE SYSTEMIC BLOOD PRESSURE AND ITS RESPONSE TO HEAD‐UP TILTING IN ANAESTHETIZED CATS

SUMMARY 1. The effects of intracisternal injections of the α‐adrenoreceptor agonists clonidine (0.2, 0.63 and 2.0μg/kg), xylazine (0.5, 8.0 and 50μg/kg), oxymetazoline (2.0 and 8.0μg/kg), noradrenaline (12.5, 50 and 100μg/kg) and α‐methylnoradrenaline (5.0 and 25;μ/kg) on mean arterial pressure and the reflex pressure responses to bilateral carotid occlusion and 45° vertical head‐up tilting have been investigated in chloralose‐urethane‐anaesthetized cats. 2. All the a‐adrenoreceptor agonists tested caused dose‐dependent reductions in mean arterial pressure ( P <0.05, Anova, d.f. = 1,58) and the reflex pressor response to bilateral carotid occlusion ( P < 0.05, Anova, d.f. = 1,58). 3. Only xylazine (50μg/kg) and noradrenaline (100μg/kg) produced a significant depression of the magnitude of the pressure compensatory response to tilting ( P <0.05, Anova, d.f. = 1, 58) whilst all the agonists tested caused an increase in the period required for pressure compensation to occur ( P <0.05, Anova, d.f. = 1,58). The action of the a‐adrenoreceptor agonists to depress mean arterial pressure and the reflex responses to bilateral carotid occlusion and tilting could be reversed by the subsequent intracisternal injection of the a‐adrenoreceptor antagonist piperoxane (50 or 100μg/kg). 5.Clonidine (0.63 μg/kg) decreased the perfusion pressure of the vascularly isolated autoperfused hindquarters ( P <0.05, Anova, d.f. = 1,19), but had no significant effect on the reflex rises in perfusion pressure evoked by bilateral carotid occlusion or tilting. Noradrenaline (50 jug/kg) significantly reduced the reflex response to tilting ( P <0.05, Anova, d.f. = 1,19), but had no effect on the other hindquarter parameters. Oxymetazoline (8.0 μg/kg) caused no significant change in any of these parameters. 6. It is concluded that intracisternally administered a‐adrenoreceptor agonists may cause some depression of orthostatic cardiovascular reflexes via a central interaction with adrenergic mechanisms.