Rats born and reared under chronically hypoxic (10% O2) conditions do not respond to acute hypoxia with an increased ventilation. Their carotid bodies undergo hyperplasia and hypertrophy and we have recently shown that K+ channels recorded in type I carotid body cells isolated from normal and chronically hypoxic (CH) rats show marked differences (Wyatt et al, 1995): normoxic type I cells express Ca2+-activated K+ (KCa) channels which are inhibited by acute hypoxia, leading to cell depolarization, opening of voltagegated Ca2+ channels (VGCCs) and the consequent influx of Ca2+ to trigger neurotransmitter release (Peers & Buckler, 1995). In type I cells from CH rats, there is far less expression of KCa channels, and, whilst the remaining K+ channels are inhibited by hypoxia, this does not lead to cell depolarization, which may explain the lack of ventilatory response to acutely inspired hypoxia in intact CH rats (Wyatt et al, 1995). An important factor in the response of normal type I cells to hypoxia is the activation of VGCCs, of which numerous sub-types exist in various tissues. It is known that L-type VGCCs are involved in hypoxic chemotransduction (Buckler & Vaughan-Jones, 1994), but very little is known about the possible presence of other VGCCs, whether they may be involved in chemotransduction, and whether they are affected by chronic hypoxia. We have therefore compared the properties of VGCCs in type I carotid body cells isolated from normoxically-reared and CH rats.