Hypoxic responses of arterial chemoreceptors in rabbits are primarily mediated by leak K channels.

The possible roles of different potassium channels in oxygen sensing mechanisms of the carotid body are still not well defined. It has been suggested that leak potassium (K(+)) channels, voltage gated K(+) channels (Kv) and Ca(2+) dependent large conductance K(+) channels (BK) play important roles in the peripheral chemo-sensing mechanisms of the carotid body. In the present study, we have made an attempt to clarify the extent to which, these channels are involved in such mechanisms using in vitro model of isolated rabbit carotid body. Selective TASK-1 channel blocker, anandamide (3 microM) induced stimulation of the carotid sinus nerve (CSN) activity, in a very similar pattern to normal hypoxic responses, with peak discharge rates of the CSN up to 63 +/- 21% of the hypoxic responses (n = 33), and no additional increase in the CSN activity was observed during the hypoxic stimulation with the co-application of anandamide (n = 6). On the other hand, inhibition of BK channels by TEA (5 mM, n = 6), was sub-maximum and typical hypoxic responses were preserved during the increased CSN activity induced by TEA (n = 7). Maximal stimulation of the CSN activity was obtained by blocking Kv channels with 4AP (2.5 mM, n = 15), which was refractory to the hypoxic response. However the hypoxic response reappeared during hyperpolarization (n = 12). We have found that the leak K(+) channels (TASK-1) seem to be importantly involved in the initiation of the oxygen sensing mechanisms of the rabbit carotid body.