Inhibition of Ca(2+)‐activated K+ currents by intracellular acidosis in isolated type I cells of the neonatal rat carotid body.

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Abstract
1. K+ and Ca2+ currents were recorded from enzymatically isolated type I cells of the neonatal rat carotid body, using the whole-cell configuration of the patch-clamp technique. The effects of intracellular acidosis, caused by bath application of anions of weak acids (propionate and acetate), were tested on these currents. 2. Bath application of propionate or acetate (10 or 20 mM) caused reversible reductions in K+ current amplitudes. These effects were maximal at low, positive test potentials where a shoulder in the current-voltage relationship occurs due to the activation of Ca(2+)-activated K+ currents. 3. Time-course studies showed propionate to cause a rapid initial reduction of K+ currents which recovered partially during its continued application. Removal of propionate produced small, transient overshoots of K+ current amplitudes. In the absence of propionate or acetate, bath application of the Na(+)-H+ exchange inhibitor amiloride caused slowly developing inhibition of K+ current amplitudes. 4. Changing extracellular pH from 7.4 to 8.0 increased K+ current amplitudes, but at this pHo propionate caused smaller reductions in K+ currents than at a pHo of 7.4. 5. In the presence of 0.1 mM-Cd2+, or in high-Mg2+ (6 mM), low-Ca2+ (0.1 mM) solutions, the residual, Ca(2+)-independent K+ currents were unaffected by 20 mM-propionate or acetate. 6. Ca2+ channel currents were also recorded, using 10 mM-Ba2+ as the charge carrier. These sustained currents were completely abolished by 0.1 mM-Cd2+ and were enlarged in the presence of 5 microM-Bay K 8644, suggesting that the currents passed through L-type Ca2+ channels. 7. Ca2+ channel currents were not significantly affected by intracellular acidosis caused by bath application of 10 mM-propionate or acetate. They were also unaffected by a reduction of the extracellular pH from 7.4 to 7.0. 8. It is concluded that intracellular acidosis selectively inhibits Ca(2+)-activated K+ currents in type I carotid body cells. The possible significance of this effect on chemotransduction in the intact carotid body is discussed.