Baroreceptor and chemoreceptor influences on sympathetic discharge to the heart

¹ Laboratory of Cardiovascular Physiology, National Heart Institute, Bethesda, Maryland

Baroreceptor and chemoreceptor influences in the regulation of sympathetic discharge to the heart were investigated, utilizing electroneurographic recordings from the left inferior cardiac nerve in the cat. Spontaneous discharge patterns exhibited phasic inhibition with the heartbeat and with inflation of the lungs. This was shown to be the consequence of baroreceptor and afferent vagal activity, respectively. Increasing blood pressure with epinephrine or angiotensin II caused marked inhibition of discharge which was abolished by baroreceptor deafferentation. No increase of cardiac sympathetic discharge occurred after the introduction of hypoxic blood into the isolated carotid sinus. Systemic hypoxia caused a marked increase in sympathetic discharge to the heart despite a large increase of systemic blood pressure. This response persisted after denervation of the peripheral chemoreceptors. A similar but less pronounced response to systemic hypercapnia was found. Systemic hypoxia frequently produced bradycardia which could be converted to tachycardia by atropine. This was associated with a large and continuous increase of cardiac sympathetic discharge to the heart. It is concluded that in systemic hypoxia both sympathetic and parasympathetic discharge to the heart is enhanced.

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