Stimulation of rat renal phosphoenolpyruvate carboxykinase activity after an intravenous lactic acid load

Abstract

It is well known that metabolic acidosis attained by ammonium chloride administration leads to an increase in renal gluconeogenesis [ 1,2] through the activation of phosphoenolpyruvate carboxykinase (EC 4.1.1.32) (PEPCK) [3-51. We have reported that muscular exercise (swimming in water at 22” C for 2 h) results in an increase of renal gluconeogenic ability and PEPCK activity, most probably as a result of the metabolic acidosis caused by overproduction of lactate [6-91. To obtain further information about the relations between lactic acidosis and renal metabolism we produced experimental lactic acidosis which could mimic in some way the physiological acidosis accompanying exercise. Then we have studied the activity of PEPCK, the gluconeogenic ability in kidney cortex and the renal content of some intermediates of gluconeogenesis from rats loaded intravenously with lactic acid or sodium lactate. We have also studied the renal response to the infusion of adrenaline, because of the involvement of this hormone in the metabolic events during exercise [lo]. Our results indicate that induction of renal PEPCK is closely related to acidosis.