Copeptin, a surrogate marker of arginine8 vasopressin, has no ability to modulate human and mouse gastric motility

Copeptin, a glycosylated peptide fragment derived from the C-terminal region of the precursor of arginine(8) vasopressin (AVP), is co-secreted with AVP in equimolar amounts. Elevated plasma AVP modulates gastric motility so we investigated whether copeptin had a similar effect. Copeptin (10(-9) -10(-7) M), and AVP (10(-12) -10(-5) M), were evaluated for their ability to modulate spontaneous and electrically-evoked (EFS) contractions of human proximal and distal gastric circular muscle in vitro. Similar experiments were performed on the mouse stomach and we re-examined the published effect of copeptin on the mouse aorta. In the presence of tetrodotoxin (10(-6) M), atropine (10(-6) M) and L-NAME (3 x 10(-4) M), human proximal and distal stomach muscle contracted spontaneously and rhythmically as did mouse distal stomach. Copeptin (10(-9) -10(-7) M), had no effect on baseline muscle tone or myogenic spontaneous contractions of either human or mouse stomach. However, AVP concentration-dependently increased tone, amplitude and frequency of contractions in both regions of human stomach with similar potency (pEC(50) 9.0-9.5; n = 4) and threshold concentration (10(-11) -10(-19) M). AVP was similarly active in the mouse stomach. EFS-evoked cholinergic contractions (human and mouse) were unaffected by both peptides EFS-evoked relaxations of mouse stomach were unaffected by copeptin. In sub-maximally contracted mouse aorta the elevated tone was unaffected by copeptin (10(-7) M) (cf. previously published study) but was reduced by carbachol (10(-6) M) and sodium nitmprusside (10(-3) M). We conclude that in contrast to AVP, copeptin over a concentration range reported in the plasma has no direct ability to modulate the motility of the human and mouse stomach.

Automated summary

The study found that, unlike AVP, copeptin does not have a direct ability to modulate the motility of the human and mouse stomach.