Vasopressin increases urinary albumin excretion in rats and humans:: involvement of V2 receptors and the renin-angiotensin system
Vasopressin increases urinary albumin excretion in rats and humans:: involvement of V2 receptors and the renin-angiotensin system
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DOI:
10.1093/ndt/18.3.497
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发表时间:
2003-03-01
影响因子:
6.1
通讯作者:
Bankir, L
中科院分区:
文献类型:
--
作者:
Bardoux, P;Bichet, DG;Bankir, L
Background. An increase in urinary albumin excretion (UAE) represents an early predictor of glomerular damage in diabetes mellitus (DM) and a risk factor for cardiovascular complications in hypertension. Vasopressin is elevated in DM and in some forms of hypertension. Previous studies in rats suggested that this hormone could play a role in the albuminuria observed in chronic renal failure or diabetic nephropathy, but no information is available concerning the mechanism of these effects and the possible influence of vasopressin on UAE in the healthy kidney. The present study was thus designed to evaluate whether vasopressin influences UAE in normal rats and humans, whether this effect is V(2)-receptor-dependent, and whether it is mediated by the renin-angiotensin system.Methods. UAE was measured in normal Wistar rats and healthy humans, or in subjects with various forms of diabetes insipidus (DI), before and after acute or chronic infusion of the vasopressin V(2) receptor agonist dDAVP(R). Chronic dDAVP administration was also performed in normal Wistar rats previously submitted to either chronic angiotensin-converting enzyme inhibition (ACEI) or chronic blockade of AT1 receptors (ARB).Results. In rats, acute or chronic dDAVP infusion increased UAE significantly and reversibly (4-fold and 6-fold, respectively). In healthy subjects, acute infusion of dDAVP tripled UAE (P