Dehydration natriuresis in male rats is mediated by oxytocin
Dehydration natriuresis in male rats is mediated by oxytocin
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DOI：
10.1152/ajpregu.1996.270.2.r427
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发表时间：
1996-02-01
影响因子：
2.8
通讯作者：
Sjoquist, N
中科院分区：
文献类型：
--
作者：
Huang, W;Lee, SL;Sjoquist, N
在先前的大鼠研究中，我们证明了与依赖于容量刺激的利钠机制不同的调节性利钠机制的存在。同时，我们发现催产素（OT）受体是高钠血症引起的促钠排泄的重要介质，而不是等渗扩容引起的促钠排泄的重要介质。在本研究中，OT在脱水尿钠排泄中的作用在清醒大鼠中进行了研究。脱水24小时引起高钠血症（从142.1 +/- 0.4至147.7 +/- 0.7 mmol/l）和尿钠排泄，并伴有类似于30%的摄食量自发减少。结合循环加压素增加引起的肾水潴留，尿钠排泄和可能的食物摄入减少有助于抵消体液渗透压的升高。尿钠排泄不能完全解释为血浆醛固酮减少。在脱水24小时结束时，血浆OT浓度从15.5 +/- 1.2增加到23.8 +/- 2.0 pg/ml。用渗透压微型泵静脉输注选择性OT受体拮抗剂[Mpa（1），D-Tyr（Et）（2），Thr（4），Orn（8）]-OT可防止脱水尿钠排泄。它的结论是，在脱水诱导的高钠血症状态OT释放，诱导钠尿和促进钠稳态。这一机制由Na+受体激活，但主要不依赖于容量状态。
In a previous study in rats we demonstrated the existence of osmoregulatory natriuretic mechanisms distinct from the natriuretic mechanisms that are dependent on volume stimulation. At the same time, we found that oxytocin (OT) receptors were important mediators of natriuresis induced by hypernatremia but not of that induced by isotonic volume expansion. In the present study, the role of OT in dehydration natriuresis was examined in conscious rats. Dehydration for 24 h caused hypernatremia (from 142.1 +/- 0.4 to 147.7 +/- 0.7 mmol/l) and natriuresis accompanied by an similar to 30% spontaneous reduction of food intake. In conjunction with renal retention of water caused by an increase in circulating vasopressin, the natriuresis and probably the reduction of food intake can help to counteract the rise in body fluid osmolality. This natriuresis could not be fully explained by the reduction in plasma aldosterone. Plasma OT concentration had increased from 15.5 +/- 1.2 to 23.8 +/- 2.0 pg/ml at the end of 24 h of dehydration. Intravenous infusion of a selective OT-receptor antagonist [Mpa(1),D-Tyr(Et)(2),Thr(4),Orn(8)]-OT using osmotic minipumps prevented dehydration natriuresis. It is concluded that in a dehydration-induced hypernatremic state OT is released, inducing natriuresis and facilitating sodium homeostasis. This mechanism is activated by Na osmoreceptors, but is not primarily dependent on the volume status.