Role of catecholamines in the control of newborn kidney adenine nucleotide content.
During the 1st h of extrauterine life, the adenine nucleotide content of the rat kidney is modified: the ATP level increases (+30%) while ADP and AMP are lowered (-30 and -50%, respectively). This leads to a high value of energy charge in the newborn kidney (0.89 vs. 0.80 in the fetus). It was possible to obtain in utero a similar modification of ATP, ADP, AMP concentrations by injections to the fetuses of cAMP, dibutyryl cAMP, or isoprenaline. Conversely, the postnatal changes in adenine nucleotide content could be prevented by administration to the fetus, just before birth, of beta- or beta 1-adrenoreceptor antagonists. Therefore the rise of kidney energy charge following parturition appears to be under hormonal control. Glucagon had no effect on kidney adenine nucleotide content. It is strongly suggested that the catecholamines released at the time of parturition are the triggering factor of this evolution.
D000227:Adenine Nucleotides / Q000378:metabolism*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D003994:Bucladesine / Q000494:pharmacology; D002395:Catecholamines / Q000502:physiology*; D000242:Cyclic AMP / Q000494:pharmacology; D004734:Energy Metabolism; D005333:Fetus / Q000187:drug effects / Q000378:metabolism; D005934:Glucagon / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D007668:Kidney / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D000227:Adenine Nucleotides; D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D003994:Bucladesine; D005934:Glucagon; D000242:Cyclic AMP; D007545:Isoproterenol