CAROTID-BODY NORADRENERGIC SENSITIVITY IN VENTILATORY ACCLIMATIZATION TO HYPOXIA

Norepinephrine inhibits ventilation in awake goats under normoxic, resting conditions. This inhibition is carotid body (CB) mediated and may be due to stimulation of noradrenergic receptors on the CB. Cao et al. (FASEB J. A118, 1991) recently suggested that CB noradrenergic receptors may be down regulated following 24-36 hours of hypoxic exposure in cats. Our study was aimed at determining whether a change in noradrenergic receptor sensitivity during ventilatory acclimatization to hypoxia (VAH) was responsible for the increased sensitivity of the CB to hypoxia during prolonged exposure to hypoxia in goats. We tested this hypothesis using intracarotid infusions of norepinephrine (NE) (0.5, 1.0, 5.0 mug.kg-1.min-1) and dopamine (DA) (1.0 mug.kg-1.min-1) in awake goats under control normoxic conditions, during 4 h of isocapnic hypoxia, and upon return to normoxia. NE and DA (1.0 mug.kg-1.min-1) both inhibited control ventilation significantly during the intracarotid infusions (56% and 62% decreases, respectively). No significant differences were found between the pre- and post-hypoxic infusions of NE and DA in normoxia, During hypoxia, inhibition of VE during NE and DA infusions was attenuated relative to control. Time-dependent changes of the NE response were not apparent during the acclimatization period suggesting that a decreased carotid body chemoreceptor sensitivity to NE and DA is not responsible for the increased drive to breathe characteristic of ventilatory acclimatization to hypoxia.