Endocrine Abstracts

Context: Osmotic stimulus or stress results in release of vasopressin. Animal studies have shown that inflammatory parameters such as interleukin-6 (IL-6) and interleukin-8 (IL-8) increase in parallel, mainly in central brain regions. Whether osmotic stimulation leads to an inflammatory response in humans is unknown. We therefore investigated the influence of osmotic stimulation on the inflammatory system in healthy volunteers.

Method: In this prospective cohort study, 44 healthy volunteers underwent a standardized test protocol leading to an osmotic stimulation into the hypertonic range by hypertonic-saline infusion (serum sodium >150 mmol/l). Copeptin, a marker to indicate vasopressin activity, sodium, osmolality, IL-6, IL-8 and TNF-a was measured at baseline and directly after osmotic after stimulation.

Results: Median serum sodium increased from 141 mmol/l (IQR 140, 142) to 151 mmol/l (IQR 150; 153) (P-value <0.01), median serum osmolality increased from 295 mmol/l (IQR 291; 298) to 315 mmol/l (312; 317) (P-value <0.01). Copeptin increased form 4.3 pg/l (IQR 3.3; 6.7) to 28.8 pg/l (19.9; 43.4) (P-value <0.01). IL-8 levels decreased from 0.79 pg/ml (IQR 0.65; 1.1) to 0.7 pg/ml (IQR 0.57; 0.9) (P-value 0.09) and TNF-a decreased from 0.53 pg/ml (IQR 0.38; 0.69) to 0.45 pg/ml (IQR 0.3; 0.5) (P-value 0.036). There was no significant change in IL-6 levels.

Conclusions: Contrary to animal data, inflammatory markers remain unchanged or decrease in human serum after osmotic stimulation. Increased vasopressin/copeptin seems not to stimulate inflammatory markers; whether a negative feedback exists remains unclear.