OXYTOCIN PRODUCES NATRIURESIS IN RATS AT PHYSIOLOGICAL PLASMA-CONCENTRATIONS
OXYTOCIN PRODUCES NATRIURESIS IN RATS AT PHYSIOLOGICAL PLASMA-CONCENTRATIONS
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DOI：
10.1210/endo-128-3-1317
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发表时间：
1991-03-01
期刊：
影响因子：
4.8
通讯作者：
STRICKER, EM
中科院分区：
文献类型：
--
作者：
VERBALIS, JG;MANGIONE, MP;STRICKER, EM
已知催产素（OT）在大剂量给药时会刺激大鼠的尿钠排泄，从而产生高血浆水平。 我们研究了生理血浆OT水平对肾钠排泄的影响，通过在清醒的成年雄性大鼠中皮下注射不同剂量的OT来维持钠缺乏的饮食。 我们的研究结果表明，OT导致剂量相关的增加尿钠排泄在输液的第一天。 与尿钠排泄增加相关的最低血浆OT水平（5-6 pmol/L）完全在大鼠生理OT分泌的范围内。 然而，这种利钠利尿作用在随后的几天维持在钠缺乏的饮食，这表明OT诱导的利钠作用是有限的，部分受体脱敏和/或减少可交换的钠池结合分泌的对立的抗心钠尿因子，如醛固酮。 预处理与OT受体拮抗剂完全阻断尿钠排泄所产生的20 pmol/h的输液的OT，但尿钠排泄不受影响的加压素V1拮抗剂，并仅部分阻断联合加压素V1和V2拮抗剂。 与以前的研究表明，在大鼠垂体OT分泌和钠食欲之间的负相关关系，这些结果支持的假设，外周和中枢分泌的OT在一致行动，在大鼠产生负钠平衡，刺激钠排泄，同时抑制钠摄入。
Oxytocin (OT) is known to stimulate natriuresis in rats when administered in large doses that produce high plasma levels. We examined the effects of physiological plasma OT levels on renal sodium excretion by infusing graded doses of OT sc in conscious adult male rats maintained on a sodium-deficient diet. Our results demonstrate that OT causes a dose-related increase in urinary sodium excretion during the initial day of infusion. The lowest plasma OT levels associated with increases in urinary sodium excretion (5-6 pmol/liter) were well within the range of physiological OT secretion in rats. However, this natriuretic effect was not sustained during subsequent days of maintenance on a sodium-deficient diet, suggesting that the OT-induced natriuresis was limited in part by receptor desensitization and/or a decreased exchangeable sodium pool in combination with secretion of opposing antinatriuretic factors such as aldosterone. Pretreatment with an OT receptor antagonist completely blocked the natriuresis produced by a 20 pmol/h infusion of OT, but urinary sodium excretion was not affected by a vasopressin V1 antagonist and was blocked only partially by a combined vasopressin V1 and V2 antagonist. Together with previous studies in rats demonstrating an inverse relation between pituitary OT secretion and sodium appetite, these results support the hypothesis that peripherally and centrally secreted OT act in concert in rats to produce a negative sodium balance by stimulating sodium excretion while inhibiting sodium ingestion.