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肾去神经支配对清醒大鼠脑室内注射生物活性肽诱导的肾素释放的影响。

Effects of renal denervation on renin release induced by intracerebroventricular administration of biological active peptides in conscious rats.

作者信息

Iwata T, Hiwada K, Kokubu T

出版信息

Neuropeptides. 1985 Sep;6(5):437-43. doi: 10.1016/0143-4179(85)90142-8.

Abstract

Experiments were performed to determine whether the renal nerve mediates the renin release induced by intracerebroventricular administration of angiotensin II (ANG II), bradykinin (BK), leucine-enkephalin (Leu-ENK) and neurotensin (NT). In sham-operated rats, both ANG II and NT suppressed plasma renin activity (PRA), BK did not affect PRA, and Leu-ENK increased PRA. Renal denervation abolished the increase in PRA by Leu-ENK. Suppression of PRA by ANG II was attenuated in denervated rats. Renal denervation did not influence the renin release by BK or NT. These results suggest that the renal nerve plays an important role in elevating PRA after central stimulation by Leu-ENK. Although suppression of PRA is mainly mediated by mechanisms other than the renal nerve, the renal nerve partially participates in suppression of PRA by ANG II.

摘要

进行实验以确定肾神经是否介导脑室内注射血管紧张素 II(ANG II)、缓激肽(BK)、亮氨酸脑啡肽(Leu-ENK)和神经降压素(NT)所诱导的肾素释放。在假手术大鼠中,ANG II 和 NT 均抑制血浆肾素活性(PRA),BK 不影响 PRA,而 Leu-ENK 增加 PRA。肾去神经支配消除了 Leu-ENK 所致的 PRA 升高。在去神经支配的大鼠中,ANG II 对 PRA 的抑制作用减弱。肾去神经支配不影响 BK 或 NT 引起的肾素释放。这些结果表明,肾神经在 Leu-ENK 中枢刺激后升高 PRA 中起重要作用。虽然 PRA 的抑制主要由肾神经以外的机制介导,但肾神经部分参与 ANG II 对 PRA 的抑制作用。

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