1. Comparisons have been made between rats anaesthetized with pentobarbitone and Saffan (Glaxovet), of respiratory and cardiovascular changes evoked by (1) brief stimulation of carotid body chemoreceptors (c.b.); (2) systemic hypoxia induced by N2 breathing for 5 s; (3) brief unloading of peripheral chemoreceptors with dopamine; and (4) O2 breathing for 10 s. The results are discussed in relation to responses reported in other species. 2. Under pentobarbitone, c.b. stimulation evoked hyperventilation, tachycardia, and vasoconstriction in hindlimb muscle and renal and mesenteric circulation. The effects of vagotomy and/or of holding ventilation constant indicated that the primary cardiac response to c.b. stimulation was bradycardia which could be overcome by tachycardia, due to a reflex mediated by pulmonary stretch receptors with vagal afferents and to other secondary effects of hyperventilation. However, reflex vasodilatation initiated by hyperventilation did not modulate the chemoreceptor-induced peripheral vasoconstriction. 3. Under light pentobarbitone, N2 evoked a similar pattern of response to c.b. stimulation, except that the tachycardia apparently also reflected the known effects of increased central inspiratory drive and central nervous hypoxia on cardiac vagal and sympathetic activity. However, under deep pentobarbitone or after guanethidine, N2 induced generalized vasodilatation. It is proposed that these responses reflected the local vasodilator actions of hypoxia. 4. Under light Saffan anaesthesia, both c.b. stimulation and N2 evoked the autonomic components of the alerting stage of the defence response which includes tachycardia and vasodilatation in hindlimb muscle, which are not secondary to hyperventilation, with renal and mesenteric vasoconstriction, pupillary dilatation and exophthalmus. However, under deep Saffan anaesthesia, c.b. stimulation and N2 produced the patterns of response they each evoked under deep pentobarbitone. It is proposed that light Saffan anaesthesia allows chemoreceptor stimulation to activate the defence areas and that under such conditions the primary response to c.b. stimulation and direct effects of hypoxia may be overridden. 5. Under pentobarbitone or Saffan, the hypoventilation induced by I.V. dopamine and by O2 indicated that almost 50% of eupnoeic ventilation was due to drive from peripheral chemoreceptors. This drive apparently played no significant role in setting the baseline level of heart rate, but could account for 10% of total peripheral resistance and of the baseline level of arterial pressure under Saffan, rather less under pentobarbitone.