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

Abstract

1. 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 P(O2). 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 K+(o) (P > 0.40). The rightward position of the response curves, as quantified by the P(O2) 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 P(O2) (P > 0.90). 3. Increasing P(O2) in hyperoxia increased chemoreceptor discharge linearly at all levels of [K+](o). Whilst discharge at any level of P(CO2) was elevated by increased levels of [K+](o), raising [K+](o) did not increase CO, sensitivity (P > 0.20). Similarly, increasing P(CO2) did not increase chemosensitivities to [K+](o). The lack of effect of [K+](o) upon CO2 chemosensitivity was also observed as P(O2) was decreased to hypoxic levels (P > 0.10). 4. Our data demonstrate that an elevation of [K+](o) can increase chemoreceptor discharge in the in vitro carotid body in a P(O2)- and P(CO2)-independent manner, suggesting that the P(O2)-dependent effects of [K+](o) previously reported in vivo may be due to other indirect effects of [K+](o) or hypoxia.