Abstract
Substitution of K + or choline for Na + in Krebs-Ringer bicarbonate buffer increased basal glucose oxidation and 3H-adenine incorporation into 3H-CAMP but had no effect on CAMP concentrations. In high K + buffer, TSH (3 mU/ml and 50 mU/ml) and prostaglandin E 1 (PGE 1) (0.1 μg/ml and 10 μg/ml) had little or no effect on glucose oxidation while their stimulation of 3H-CAMP formation and CAMP levels was equivalent to that obtained using regular Krebs-Ringer bicarbonate buffer. These results indicated that high K + inhibited the effects of CAMP and not its generation. The increased basal glucose oxidation in high K + buffer probably reflected increased membrane permeability since slices incubated with 14C-1-glucose and regular Krebs-Ringer bicarbonate buffer did not have augmented 14CO 2 production when they were later transferred to high K + buffer. The increased 3H-adenine incorporation into 3H-CAMP cannot be explained by increased membrane permeability, but appeared to reflect an effect on the intracellular conversion of 3H-adenine to 3H-ATP or 3H-ATP to 3H-CAMP. The effect of high K + probably reflected low Na + in the buffer since similar results were obtained when choline chloride was substituted for NaCl in Krebs-Ringer bicarbonate buffer. Exclusion of Ca ++ from Krebs-Ringer bicarbonate buffer decreased basal glucose oxidation, but had no effect on 3H-adenine conversion to 3H-CAMP or CAMP concentrations. Although effects of TSH and PGE 1 on glucose oxidation were diminished in buffer devoid of Ca ++, their stimulation of 3H-CAMP formation and CAMP levels was similar in the presence and absence of Ca ++. These results demonstrate that changes in the ionic composition of the buffer do not interfere with activation of the adenyl cyclase-CAMP system but modify some of the subsequent actions of the CAMP formed.
Published Version
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