Cardioventilatory responses to hypoxia, the O2 chemoreceptor stimulant sodium cyanide (NaCN), and intra-arterial injection of atropine, noradrenaline and DL-propranolol were investigated in the adriatic sturgeon. Hypoxia elicited a bradycardia and hyperventilation. 1 mg NaCN added to water entering the buccal cavity stimulated a transient bradycardia but intra-arterial infusion of 150 micrograms NaCN did not, indicating that hypoxic bradycardia is controlled by chemoreceptors sensitive only to water O2 levels. NaCN stimulated hyperventilation both when added to the water and when infused intra-arterially, indicating that hypoxic hyperventilation is controlled by chemoreceptors sensitive to both internal and external milieux. Atropine abolished the hypoxic bradycardia and returned heart rate to normoxic values indicating that this species has no inhibitory vagal tone in normoxia. Noradrenaline stimulated ventilation, an effect abolished by DL-propranolol. Propranolol blocked ventilatory responses to intra-arterial infusion of NaCN whereas responses to NaCN added to the water remained unaffected, indicating that propranolol may inhibit internally-oriented O2-chemoreceptor activity or that ventilatory responses to intra-arterial NaCN are stimulated by a release of circulating catecholamines. Cardioventilatory control systems in sturgeon are similar to those of other actinopterygians but also show some characteristics of the system described for elasmobranchs.

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