These authors contributed equally to this manuscript.
Arginine vasopressin-dependent and AVP-independent mechanisms of renal fluid absorption during thirsting despite glucocorticoid-mediated vasopressin suppression
Article first published online: 25 JAN 2013
© 2012 Blackwell Publishing Ltd
Volume 78, Issue 3, pages 431–437, March 2013
How to Cite
Ufer, F., Diederich, S., Pedersen, E. B., Spranger, J., Pfeiffer, A. F. H., Bähr, V. and Mai, K. (2013), Arginine vasopressin-dependent and AVP-independent mechanisms of renal fluid absorption during thirsting despite glucocorticoid-mediated vasopressin suppression. Clinical Endocrinology, 78: 431–437. doi: 10.1111/cen.12006
- Issue published online: 25 JAN 2013
- Article first published online: 25 JAN 2013
- Accepted manuscript online: 8 AUG 2012 02:19AM EST
- Manuscript Accepted: 2 AUG 2012
- Manuscript Revised: 16 JUL 2012
- Manuscript Revised: 1 JUL 2012
- Manuscript Received: 8 JUN 2012
Glucocorticoids seem to modify the release and effects of plasma arginine vasopressin (pAVP). However, underlying processes are not well understood. This study aimed to evaluate the mechanism of the modulating effects of glucocorticoids on pAVP and renal water reabsorption.
Fluid deprivation tests were performed without (d0) and after one (d1) and five days (d5) of oral prednisolone (Pred) pretreatment in a dosage relevant to drug therapy (30 mg/day).
Twelve healthy male volunteers participated in this trial.
Plasma and urinary osmolality, pAVP, renin, aldosterone, plasma atrial natriuretic peptide (ANP) as well as urinary secretion of aquaporin-2 (AQP2) and prostaglandin E2 (PGE2) were analysed.
An appropriate rise in pAVP was observable during thirsting (P < 0·001), which was absent after Pred pretreatment. However, the plasma and urinary osmolality after Pred treatment did not differ when compared with the basal thirsting test. Unchanged urinary AQP2 excretion suggests AVP-independent mechanisms of renal fluid reabsorption. Plasma renin concentration as well as ANP was substantially increased after Pred intake at d1 and d5 (both P < 0·05), which may mediate such AVP-independent mechanisms. Urinary PGE2 secretion was not influenced by Pred pretreatment, making a PGE2-mediated effect on renal AQP2 translocation and water permeability unlikely. Increased efficacy of exogenous desmopressin at d1 and d5 indicates also a relative increase in AVP sensitivity of the tubular cells after Pred intake.
The here presented data are compatible with an increased AVP sensitivity and a partially AVP-independent regulation of AQP2 translocation and renal fluid reabsorption during glucocorticoid treatment.