PH REGULATION IN ADULT-RAT CAROTID-BODY GLOMUS CELLS - IMPORTANCE OF EXTRACELLULAR PH, SODIUM, AND POTASSIUM

The course of intracellular pH (pH(i)) was followed in superfused (36-degrees-C) single glomus (type I) cells of the freshly dissociated adult rat carotid body. The cells had been loaded with the pH-sensitive fluorescent dye 2',7'-(2-carboxyethyl)-5 (and -6)-carboxyfluorescein. The high K+-nigericin method was used for calibration. The pH(i) of the glomus cell at pH(o) 7.40, without CO2, was 7.23 +/- 0.02 (n = 70); in 5% CO2/25 mM HCO3-, pH(i) was 7.18 +/- 0.08 (n = 9). The pH(i) was very sensitive to changes in pH(o). Without CO2, DELTApH(i)/DELTApH(o) was 0.85 (pH(o) 6.20-8.00; 32 cells), while in CO2/HCO3- this ratio was 0.82 irrespective of whether pH(o) (6.80-7.40; 14 cells) was changed at constant PCO2 or at constant [HCO3-]o. The great pH(i) sensitivity of the glomus cell to pH(o) is matched only by that of the human red cell. An active Na+/H+ exchanger (apparent K(m) = 58 +/- 6 mM) is present in glomus cells: Na+ removal or addition of the amiloride derivative 5-(N,N-hexamethylene)-amiloride induced pH(i) to fall by as much as 0.9. The membrane of these cells also contains a K+/H+ exchanger. Raising [K+]. from 4.7 to 25, 50, or 140 mM reversibly raised pH(i) by 0.2, 0.3, and 0.6, respectively. Rb+ had no effect, but in corresponding concentrations of Tl+ alkalinization was much faster than in K+. Reducing [K+]o to 1.5 mM lowered pH(i) by 0.1. These pH(i) changes were shown not to be due to changes in membrane voltage, and were even more striking in the absence of Na+. Intrinsic buffering power (amount of strong base required to produce, in the nominal absence of CO2, a small pH(i) rise) increased from 3 to approximately 21 mM as pH(i) was lowered, but remained nearly unchanged below pH(i) 6.60. The fitted expression assumed the presence of one "equivalent" intracellular buffer (pK 6.41, 41 mM). The exceptional pH(i) sensitivity to pHo suggests that the pH(i) of the glomus cell is a link in the chemoreceptor's response to external acidity.