Metabolic activities and their responses to
catecholamines were studied in fasted rats exposed to simulated altitudes. Analysis of hepatic levels of gluconeogenic intermediates revealed the inhibition of gluconeogenesis between
glyceric acid 3-P and
fructose 6-P associated with a rise of the ratios of redox pairs such as
lactate to
pyruvate in livers of alkalotic rats. Inhibition of gluconeogenesis was indicated also by the suppressed incorporation of
glutamate 14C into
blood glucose. Since no activation was detected on glycolytic pathway of skeletal muscles, marked hyperlactacidemia during
alkalosis appeared to result from the suppression of hepatic gluconeogenesis. Most of metabolic actions of
epinephrine and isoproterenal known to be mediated via the beta receptor were significantly reduced but not completely abolished during
alkalosis. Exceptionally,
hyperinsulinemia induced by
isoproterenol was completely reversed and replaced by hypoinsulinemia during
alkalosis. Despite hypoinsulinemia,
hyperglycemia induced by
glucose load decreased more rapidly in alkalotic than in normal rats. In view of the fact that the
adrenergic alpha receptor is involved in theinhibition of insulin secretion, the observed irregular modifications of
catecholamine actions could be explained on the basis of a postulate that the
adrenergic alpha-receptor functions are potentiated in
alkalosis.