Effect of chronic hyponatremia on central and peripheral oxytocin and vasopressin secretion in rats.
Effect of chronic hyponatremia on central and peripheral oxytocin and vasopressin secretion in rats.
复制标题
慢性低钠血症对大鼠中枢和外周催产素和加压素分泌的影响。
DOI：
10.1159/000126863
复制
发表时间：
1995
影响因子：
4.1
通讯作者：
Verbalis,JG
中科院分区：
文献类型：
--
作者：
Iványi,T;Dohanics,J;Verbalis,JG
先前的研究表明，许多刺激垂体外周分泌催产素（OT）和加压素（AVP）的治疗同时增加了脑脊液（CSF）中这些肽的水平。由于在低钠血症大鼠中，垂体刺激的OT和AVP分泌明显减弱，因此本研究评估了在持续低钠血症期间，中枢OT和AVP分泌到CSF中是否同样受到抑制。用皮下注射法使成年雄性大鼠枕大池插管出现低钠血症（血浆[Na+] <110 mmol/l）。输注去氨加压素（dDAVP; 10 ng/h）并摄入流质饮食3天，然后进行渗透性（i. v.或i. p.注射2 MNaCl; HS）或非渗透性（6 mmol/kg的0.15MLiCl i. p.）刺激.在正常钠血症大鼠静脉注射和腹腔注射HS引起血浆OT和AVP水平显着增加治疗后30分钟。CSF中OT显著升高，但AVP未显著升高。尽管血浆Na+浓度增加相似，但低钠血症大鼠的血浆OT反应在HS i. v.后不存在，并且在HS i. p.后显著减弱，但两组血浆AVP均未升高。与血浆结果平行，静脉注射HS的低钠血症大鼠中不存在CSF OT反应，腹腔注射HS的低钠血症大鼠中CSF OT反应显著减弱，但两组均未出现CSF AVP升高。用等渗LiCl非渗透刺激治疗后20 min，正常血钠大鼠血浆和CSF中OT水平均升高。尽管低钠血症大鼠血浆OT反应显著减弱，但CSF OT反应的等效降低未达到统计学显著性。这些结果表明，持续的低钠血症抑制中枢和神经垂体OT分泌的急性渗透刺激。高渗和低渗条件下CSF和血浆OT水平的平行变化支持渗透刺激期间发现的CSF OT增加是大细胞来源的可能性，可能反映了树突状细胞释放。在低钠血症大鼠中腹膜内注射HS和LiCl后观察到的血浆和CSF OT反应的不完全抑制进一步表明，非渗透性传入输入可以覆盖大细胞OT神经元的渗透抑制。
Previous studies have shown that many treatments that stimulate the peripheral secretion of oxytocin (OT) and vasopressin (AVP) from the pituitary simultaneously increase the levels of these peptides in the cerebrospinal fluid (CSF). Since osmotically and nonosmotically stimulated pituitary secretion of OT and AVP is markedly blunted in hyponatremic rats, the present studies evaluated whether central OT and AVP secretion into the CSF is similarly inhibited during sustained hyponatremia. Adult male rats with indwelling cisterna magna cannulae were rendered hyponatremic (plasma [Na+] <110 mmol/l) by s.c. infusion of desmopressin (dDAVP; 10 ng/h) in combination with ingestion of a liquid diet for 3 days, then subjected to osmotic (i.v. or i.p. injection of 2MNaCl; HS) or nonosmotic (6 mmol/kg of 0.15MLiCl i.p.) stimulation. In normonatremic rats both i.v. and i.p. HS caused marked increases in plasma OT and AVP levels 30 min after treatment. Significant elevations of OT, but not AVP, were also present in CSF. Despite similar increases in plasma Na+concentrations, plasma OT responses in the hyponatremic rats were absent after HS i.v. and were significantly blunted after HS i.p., but neither group had increased plasma AVP. In parallel with the plasma results, CSF OT responses were absent in hyponatremic rats given HS i.v. and significantly blunted in hyponatremic rats given HS i.p., but neither group had increased CSF AVP. Nonosmotic stimulation with isotonic LiCl increased OT levels both in plasma and CSF in normonatremic rats 20 min after treatment. Although plasma OT responses were significantly blunted in the hyponatremic rats, the equivalent decreases in the CSF OT responses did not reach statistical significance. These results demonstrate that sustained hyponatremia inhibits both central and neurohypophyseal OT secretion in response to acute osmotic stimuli. The parallel changes in CSF and plasma OT levels under hyperosmolar and hypoosmolar conditions supports the likelihood that the increased CSF OT found during osmotic stimulation is of magnocellular origin, possibly reflecting dendritic release. The incomplete inhibition of plasma and CSF OT responses seen after i.p. injection of HS and LiCl in hyponatremic rats further indicates that nonosmotic afferent inputs can override osmotic inhibition of magnocellular OT neurons.