In vitro recording of chemoreceptor activity in catecholamine-depleted rabbit carotid bodies.

Carotid bodies, together with Hering's nerves, were excised from anesthetized rabbits 24, 48 or 72 h after single reserpine injections (5 mg kg-1, i.v. or i.p.) and were superfused in vitro. Some carotid bodies were processed for formaldehyde-induced fluorescence microscopy to assess catecholamine depletion. Twenty-four hours after reserpine treatment, most of the type I cell islets had lost their fluorescence and the number of spontaneously active chemoafferent units was dramatically reduced. Forty-eight hours after reserpine injection, both the fluorescence of type I cells had partially recovered and the number of chemoreceptor units was almost normal. A significant reduction of both the normoxic and hypoxic frequencies of discharge was demonstrated in carotid bodies examined 24 or 48 h after reserpine pretreatment. Superfusions with dopamine (1, 10, 100 microM) transiently restored the response to hypoxia. It is proposed that catecholamines contained in type I cells play a prominent role in the genesis of chemoafferent activity and in the chemoreceptor response to hypoxia.