The kidneys stimulate vasopressin release during hemorrhage in rats with chronic NTS lesions.
The kidneys stimulate vasopressin release during hemorrhage in rats with chronic NTS lesions.
复制标题
在患有慢性 NTS 损伤的大鼠出血过程中，肾脏会刺激加压素的释放。
DOI：
10.1152/ajpregu.1997.272.5.r1540
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Sved,AF
中科院分区：
文献类型：
--
作者：
Schreihofer,AM;Hoffman,GE;Sved,AF
消除慢性损毁孤束核(NTS)对脑的压力感受性传入不会改变清醒大鼠低血压出血时血管加压素(VP)的释放。为了研究肾脏在慢性NTS大鼠出血时是否在刺激VP释放中起关键作用，我们检测了去除来自肾脏的潜在信号的效果。在NTS损毁的大鼠，肾切除或去神经，而不是卡托普利注射，显著减弱(但不能取消)失血诱导的VP释放。相反，这些手法都没有减弱NTS完整大鼠的VP反应。失血使对照组和NTS损伤组大鼠血浆肾素活性升高，这种反应不受去肾神经支配的影响。在NTS损伤和肾失神经的大鼠，失血诱导下丘脑大细胞VP神经元Fos的表达，其模式与完整大鼠的失血相似。总之，这些结果表明，在慢性NTS损伤的大鼠中，来自肾脏的传入信号在出血时刺激VP的释放，可能是通过肾神经。然而，在NTS完整或选择性移除动脉压力感受器输入后，对肾脏的这种作用并不明显。此外，在没有NTS和肾神经的情况下，低血压出血产生的另一个信号继续刺激VP神经元。
Elimination of baroreceptor afferent input to the brain produced by chronic lesion of nucleus of the solitary tract (NTS) does not alter vasopressin (VP) release during hypotensive hemorrhage in conscious rats. To investigate whether the kidneys play a critical role in stimulating VP release during hemorrhage in chronic NTS-lesioned rats, we examined the effects of removing potential signals arising from the kidneys. In NTS-lesioned rats, nephrectomy or renal denervation, but not captopril injection, markedly attenuated (but did not abolish) hemorrhage-induced VP release. In contrast, none of these manipulations attenuated the VP response in NTS-intact rats. Hemorrhage increased plasma renin activity in control and NTS-lesioned rats, and this response was not altered by renal denervation. In rats with NTS lesions and renal denervation, hemorrhage induced the expression of Fos in hypothalamic magnocellular VP neurons in a pattern similar to that of hemorrhage in intact rats. Collectively, these results indicate that in chronic NTS-lesioned rats an afferent signal arising from the kidneys stimulates VP release during hemorrhage, possibly through renal nerves. However, with the NTS intact or after the selective removal of arterial baroreceptor inputs, such a role for the kidneys is not apparent. Furthermore, in the absence of the NTS and renal nerves, another signal generated by hypotensive hemorrhage continues to stimulate VP neurons.