Engel P A, Rowe J W, Minaker K L, Robertson G L
Am J Physiol. 1984 Feb;246(2 Pt 1):E202-7. doi: 10.1152/ajpendo.1984.246.2.E202.
To characterize the influence of extracellular volume status on vasopressin pharmacokinetics, eleven young (aged 19-31 yr) and four old (aged 62-80 yr) subjects received bolus injections of 1 mU/kg Pitressin or synthetic arginine vasopressin following 6 days of sodium depletion (10 meq Na/day) or sodium loading (250 meq Na/day). In six young subjects the rapid decline in plasma vasopressin (pAVP) following the initial peak was interrupted by a second peak 5-30 pg/ml in magnitude 7.5-20 min after injection. In four of these subjects the second peak was larger following sodium depletion as compared with sodium loading. In the elderly a small (4 pg/ml) second peak was present in one sodium-depleted subject. Of five sodium-depleted subjects with central diabetes insipidus, none showed a secondary rise in pAVP. These results indicate that exogenous vasopressin may stimulate the release of endogenous AVP, an effect that appears to be enhanced by sodium depletion and is virtually absent in the elderly. There was no effect of age, volume status, or diabetes insipidus on AVP pharmacokinetics.
为了描述细胞外液容量状态对血管加压素药代动力学的影响,11名年轻受试者(年龄19 - 31岁)和4名老年受试者(年龄62 - 80岁)在经历6天的低钠(10毫当量钠/天)或高钠(250毫当量钠/天)摄入后,接受了1 mU/kg垂体后叶素或合成精氨酸血管加压素的静脉推注。在6名年轻受试者中,注射后7.5 - 20分钟,初始峰值后血浆血管加压素(pAVP)的快速下降被第二个峰值打断,第二个峰值幅度为5 - 30 pg/ml。在其中4名受试者中,与高钠摄入相比,低钠摄入后第二个峰值更大。在老年受试者中,1名低钠受试者出现了一个小的(4 pg/ml)第二个峰值。在5名患有中枢性尿崩症的低钠受试者中,没有一人的pAVP出现继发性升高。这些结果表明,外源性血管加压素可能刺激内源性AVP的释放,这种效应在低钠状态下似乎会增强,而在老年人中几乎不存在。年龄、容量状态或尿崩症对AVP药代动力学没有影响。