In cannulated trout there was no cholinergic vagal tone as revealed by atropine blockade during normal heart rates. Reductions in heart rate occasionally occurred under normoxia without apparent external stimuli ('spontaneous' bradycardia) and always occurred under environmental hypoxia (hypoxic bradycardia) due to the imposition of significant vagal tone. Direct measurements of cardiac output (Q) during these bradycardias showed that increases in cardiac stroke volume compensated for the falls in heart rate so that total Q remained unchanged or increased slightly. Sudden experimental reductions in arterial blood pressure via blockade of systemic vasomotor tone with yohimbine or via haemorrhage had no effect on heart rate during normal rates, but caused cardioacceleration during both types of bradycardia. These increases in heart rate never exceeded the point of zero vagal tone (normal heart rate) and were largely or wholly due to reductions in endogenous vagal tone. These cardioaccelerations were temporary; spontaneous bradycardia could re-occur at any time, while hypoxic bradycardia always re-occurred if the hypoxic stimulus were maintained. The results are interpreted in terms of a central interaction between the baroreceptor and chemoreceptor reflexes.