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

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.