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Endocrine Abstracts (2022) 86 P248 | DOI: 10.1530/endoabs.86.P248

SFEBES2022 Poster Presentations Neuroendocrinology and Pituitary (72 abstracts)

Vasopressin in Not a Strong Stimulus for ACTH-Cortisol Secretion In Humans

Krzysztof Lewandowski , Katarzyna Malicka & Andrzej Lewiński


Department of Endocrinology & Metabolic Diseases, The Medical University of Lodz, Lodz, Poland


Background: Vasopressin, secreted in equimolar amounts with copeptin, is implicated as a stimulus for ACTH secretion during dynamic tests, such as Glucagon Stimulation Test (GST) or Insulin Tolerance Test (ITT). Some individuals with intact ACTH-cortisol axis, demonstrate, however, a lack of further cortisol stimulation during GST. We have assessed whether failure of further ACTH-cortisol increase during GST may be associated with an inadequate vasopressin/copeptin release.

Subjects & Methods: We measured copeptin, ACTH, cortisol, glucose and growth hormone (GH) at 0, 60, 90, 120, 150 and 180 minutes during GST in ten individuals (nine female) age 41.4±15.2 years, who had satisfactory initial cortisol concentrations (mean cortisol 20.34±5.10 µg/dl), but failed to show any further cortisol increment during GST. For comparison, we measured the same parameters in two males during ITT.

Results: During GST there was a significant increase in copeptin concentrations (e.g. from 4.35±2.62 pmo/l to 6.93±3.80 pmo/l, 0 vs 180 min, P=0.02), with an average individual increase of 98% (range 10% to 321%). There was a robust increase in GH concentrations (P=0.002), and decline in cortisol (P=0.02, average decline -21.8%) and a borderline non-significant fall in ACTH concentrations (P=0.06). The relative increase in copeptin concentrations during ITT (176% and 52.2%) overlapped with individual increments observed during GST, but in contrast to GST, there was an increase of cortisol (20.45→24.26 µg/dl and 4.23→29.29 µg/dl, respectively).

Conclusions: Vasopressin/copeptin concentrations increase during GST despite the lack of an increment, or even a decline in ACTH-cortisol levels. This implies that vasopressin appears to be a rather weak stimulus for ACTH-cortisol secretion, at least in those with relatively high initial cortisol concentrations. An increase in cortisol concentrations during ITT cannot be explained by more robust vasopressin/copeptin response than during GST.

Volume 86

Society for Endocrinology BES 2022

Harrogate, United Kingdom
14 Nov 2022 - 16 Nov 2022

Society for Endocrinology 

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