Extracellular potassium and chemosensitivity in the rat carotid body, in vitro.

The effects of raising extracellular potassium concentration ([K+]o) from 3.0 to 5.3, 9.5 or 16.8 mM on chemoreceptor responses to hypoxia, hypercapnia and asphyxia were examined in a superfused in vitro rat carotid body preparation. 2. Single-exponential functions with offset were fitted to the chemoreceptor discharge responses to ramp decreases in Po2. Increasing [K+]o was without effect upon the rate constants of the fitted exponential functions (P > 0.20). Increasing [K+]o, significantly increased the horizontal asymptote (chemoreceptor discharge in hyperoxia) in a non-linear fashion when all levels of [K+]o were included in the analysis (P < 0.001) but not when a comparison was made only between 3.0 and 5.3 mM Ko+ (P > 0.40). The rightward position of the response curves, as quantified by the Po2 at 50% maximum discharge, was linearly related to [K+]o but only when all levels of [K+]o were included in the analysis (P < 0.03). Chemoreceptor sensitivity to [K+]o increased non-linearly as [K+]o was increased but this effect was not dependent upon the Po2 (P > 0.90). 4. Increasing PCO2 in hyperoxia increased chemoreceptor discharge linearly at all levels of [K+]o. Whilst discharge at any level of PCO2 was elevated by increased levels of [K+]o, raising [K+]o did not increase CO2 sensitivity (P > 0.20). Similarly, increasing PCO2 did not increase chemosensitivity to [K+]o. The lack of effect of [K+]o upon CO2 chemosensitivity was also observed as Po2 was decreased to hypoxic levels (P > 0.10). 5. Our data demonstrate that an elevation of [K+]o can increase chemoreceptor discharge in the in vitro carotid body in a PO2- and PCO2-independent manner, suggesting that the PO2-dependent effects of [K+]o, previously reported in vivo may be due to other indirect effects of [K+]o or hypoxia.