Potentiation of the action of the vagus nerve on the heart in severe hypoxia

Arterial hypoxia stimulates the peripheral chemoreceptors. Such stimulation can cause reflex slowing of the heart, particularly when secondary effects of increased ventilation are prevented. The bradycardia is mediated by the vagus nerves as it is abolished or greatly attenuated by vagotomy or administration of atropine. Furthermore, increased efferent neural activity has been recorded directly from the cardiac vagus in hypoxia. Thus, it has been widely assumed that the bradycardia occurring in hypoxia is solely the result of such increases in efferent activity in the vagus nerve. The results reported here indicate that a potentiation by hypoxia of the effects of vagal impulses arriving at the heart can also contribute to the response, particularly when hypoxia is severe.