Orally Administered Prednisolone Decreases Plasma Arginine Vasopressin and Serum Copeptin Concentrations in Healthy Dogs
Overview
Affiliations
Background: The pathophysiology of polyuria and polydipsia secondary to exogenous glucocorticoid excess is incompletely understood.
Objective: Investigate plasma AVP (pAVP) and serum CoP (sCoP) concentrations in healthy dogs before, during, and after abrupt discontinuation of a long-term course of orally administered prednisolone.
Animals: Eight healthy neutered young adult research Beagles.
Methods: In our prospective longitudinal study, Beagles were treated with a placebo PO q24h for 15 days (baseline), followed by a 35-day course of prednisolone (2.35-2.75 mg/kg PO q24h) and then abrupt discontinuation of prednisolone. Serial pAVP and sCoP concentrations, urine specific gravity (USG) and calculated plasma osmolality (pOsm) were determined during placebo and prednisolone administration, and up to 4 weeks after prednisolone discontinuation. Paired plasma samples for pAVP measurement were obtained in EDTA tubes with (pAVP) and without (pAVP) a proprietary combination of protease, esterase, and dipeptidyl peptidase-IV inhibitors (BD Biosciences P800).
Results: Mean pAVP and sCoP concentrations were significantly lower at the end of the prednisolone course (25.8 ± 8.1 pg/mL and 166 pg/mL, range, 131-223) vs baseline (34.1 ± 5.4 pg/mL and 243 pg/mL, range, 157-336; P = .02, P = .02, respectively). Correlations between pAVP and sCoP (r = .77, P = .001) and pAVP and USG (r = .61, P = .02) were positive, despite no correlation between pAVP and pOsm, sCoP and pOsm, and sCoP and USG. On paired samples, mean pAVP was significantly lower (5.0 ± 2.5 pg/mL) than mean pAVP (34.1 ± 5.4 pg/mL; P < .0001).
Conclusions And Clinical Importance: Orally administered prednisolone led to markedly decreased plasma AVP and serum CoP concentrations despite increased calculated plasma osmolality and stable systolic blood pressure.
Paulin M, Mehrabanpour D, Unniappan S, Snead E J Vet Intern Med. 2025; 39(1):e17304.
PMID: 39831546 PMC: 11744477. DOI: 10.1111/jvim.17304.