Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 21 P292


Circadian and pulsatile secretion of copeptin, an arginine vasopressin (AVP) marker, argues against a physiological role of AVP in cortisol release

Ken Darzy1, Kashinath Dixit2, Stephen Shalet2, Nils Morgenthaler3 & Georg Brabant2

1Department of Endocrinology, Queen Elizabeth II Hospital, Welwyn Garden City, Hertfordshire, UK; 2Department of Endocrinology, Christie Hospital, Manchester, UK; 3Research Department, BRAHMS, AG, Berlin, Germany.

Copeptin is a stable AVP marker and stoichiometrically released with AVP. It closely reflects changes in water balance. Its stimulation in severe stress has recently has been suggested for the early diagnosis of myocardial infarction but clear definition of the physiological variability is necessary. Here, we studied the pulsatile and circadian variation in healthy individuals and compared copeptin to cortisol rhythms.

Copeptin levels were sampled every 20 min for 24 h starting at 0900 h in a series of seven healthy subjects (one female; age 18–37 years, mean BMI 22.6 kg/m2). Serum copeptin was measured with a specific immunoassay (detection limit of 1.7 pmol/l), cortisol by a commercially available assay (Bayer Corp., Pittsburgh, PA, USA). The maximal inter- and the intraassay CV are 6.5% for copeptin and 7.9% for cortisol. Cluster algorithm was used to analyse copeptin profiles.

No consistent circadian copeptin rhythm was present but pulses vary widely between individuals over the 24 h with no evidence of synchronization among subjects or a clear relation to the light–dark cycle or to cortisol secretion. Particularly the cortisol peak levels found during the second half of the night is not anteceded or otherwise reflected in copeptin release.

AVP is known to acutely stimulate cortisol in stress situations. However, our present findings argue against any important physiological role of AVP in the generation of early morning cortisol rise (circadian rhythm). Our data will further help to better define this diagnostic grey zone for using copeptin measurements in the prediction of stress conditions. Particularly, in the light of the very attractive idea to use low copeptin levels as a very early negative predictor in myocardial infarction this physiological variation of copeptin have to be considered.

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