Abstract

1. To examine the correlation between chemosensory response and dopamine release induced by hypoxic stimulation, we studied carotid bodies excised from anaesthetized cats. 2. The carotid bodies with their carotid (sinus) nerves were superfused in vitro with modified Tyrode solution (pH 7.40, at 37.5°C) equilibrated with 20 or 100% O2. The PO2 of the superfusing channel was monitored polarographically. The frequency of chemosensory discharges (f(x)) was recorded from the whole carotid nerve. Catecholamine (CA) efflux mostly consisting of dopamine - was measured by high-speed chronoamperometry through Nafion-coated carbon electrodes placed on the carotid body tissue. Chemosensory stimulation was induced by intrastream injections of NaCN, by superfusion with 100% N2-equilibrated saline (lowering P(O2) to 25-40 Torr) or by flow interruption. 3. Low doses of NaCN increased f(x), but had no measurable effect on CA efflux, while larger doses produced fast increases in f(x), preceding delayed and prolonged increases in CA efflux. Repeated injections of NaCN, still increasing f(x), gave reduced CB effluxes. 4. Switching to hypoxic superfusion for 6-8 min produced large and fast f(x), increases, but delayed and prolonged augmentations of CA efflux. 5. Administration of three to four boluses of dopamine (7-15 ?g; augmenting CA concentration by up to 35 ?M) initially decreased f(x), after which hypoxic stimulation resulted in enhanced and faster CA effluxes, without changing the speed and intensity of chemosensory responses. 6. Flow interruptions induced fast increases in f(x) and delayed increases in CA efflux. Repeated flow interruptions produced similar increases in f(x) but progressively attenuated CA effluxes. 7. Our results suggest that CA efflux is not essential for hypoxia-induced chemosensory excitastion in the cat carotid body. They also suggest the presence of two pools of releasable CAs in the carotid body, one of slow turnover and release, and another of recently incorporated dopamine and fast release, both pools being rapidly depleted by repeated stimulation of the carotid body.