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一氧化氮合酶的中枢抑制作用可减弱脱水大鼠下丘脑-神经垂体系统的水摄入,但不改变增强的葡萄糖利用。

Central inhibition of nitric oxide synthase attenuates water intake but does not alter enhanced glucose utilization in the hypothalamo-neurohypophysial system of dehydrated rats.

作者信息

Kadekaro M, Terrell M L, Harmann P, Summy-Long J Y

机构信息

Division of Neurosurgery, University of Texas Medical Branch at Galveston 77555-0517.

出版信息

Neurosci Lett. 1994 May 23;173(1-2):115-8. doi: 10.1016/0304-3940(94)90162-7.

DOI:10.1016/0304-3940(94)90162-7
PMID:7523994
Abstract

I.c.v. administration of a nitric oxide (NO) synthase inhibitor (NG-monomethyl-L-arginine, NMMA, 500 micrograms/5 microliters) to conscious rats deprived of water for 24 h attenuated drinking and decreased glucose utilization in the subfornical organ and median preoptic nucleus. NMMA did not alter the enhanced glucose utilization in the hypothalamo-neurohypophysial system (HNS) of dehydrated rats, although it has been shown to increase, selectively, oxytocin (OT) secretion [18]. This suggests that NO may act in the neural lobe to inhibit OT secretion and promote the preferential release of vasopressin during dehydration. This effect is similar to the blockade of endogenous opiate receptors by naloxone.

摘要

向禁水24小时的清醒大鼠脑室内注射一氧化氮(NO)合酶抑制剂(Nω-甲基-L-精氨酸,NMMA,500微克/5微升),可减弱饮水,并降低穹窿下器和视前正中核的葡萄糖利用率。尽管已表明NMMA可选择性增加催产素(OT)分泌[18],但它并未改变脱水大鼠下丘脑-神经垂体系统(HNS)中增强的葡萄糖利用率。这表明,NO可能在神经叶中发挥作用,抑制OT分泌,并在脱水过程中促进血管加压素的优先释放。这种作用类似于纳洛酮对内源性阿片受体的阻断作用。

相似文献

1
Central inhibition of nitric oxide synthase attenuates water intake but does not alter enhanced glucose utilization in the hypothalamo-neurohypophysial system of dehydrated rats.一氧化氮合酶的中枢抑制作用可减弱脱水大鼠下丘脑-神经垂体系统的水摄入,但不改变增强的葡萄糖利用。
Neurosci Lett. 1994 May 23;173(1-2):115-8. doi: 10.1016/0304-3940(94)90162-7.
2
Central inhibition of nitric oxide synthase preferentially augments release of oxytocin during dehydration.脱水过程中,一氧化氮合酶的中枢抑制优先增强催产素的释放。
Neurosci Lett. 1993 Apr 2;152(1-2):190-3. doi: 10.1016/0304-3940(93)90515-m.
3
Centrally administered galanin modifies vasopressin and oxytocin release from the hypothalamo-neurohypophysial system of euhydrated and dehydrated rats.中枢给予甘丙肽可改变正常水合和脱水大鼠下丘脑-神经垂体系统中血管加压素和催产素的释放。
J Physiol Pharmacol. 2003 Dec;54(4):625-41.
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Indomethacin prevents the L-NAME-induced increase in plasma levels of oxytocin in dehydrated rats.吲哚美辛可预防L-硝基精氨酸甲酯诱导的脱水大鼠血浆中催产素水平升高。
Brain Res. 2000 Sep 22;877(2):371-3. doi: 10.1016/s0006-8993(00)02699-8.
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Nitric oxide control of drinking, vasopressin and oxytocin release and blood pressure in dehydrated rats.一氧化氮对脱水大鼠饮水、血管加压素和催产素释放及血压的调控
Physiol Behav. 1998 Mar;63(5):763-9. doi: 10.1016/s0031-9384(97)00528-3.
6
Nitric oxide synthase inhibitors prevent apomorphine- and oxytocin-induced penile erection and yawning in male rats.一氧化氮合酶抑制剂可阻止雄性大鼠因阿扑吗啡和催产素诱导的阴茎勃起及打哈欠。
Brain Res Bull. 1993;32(1):71-4. doi: 10.1016/0361-9230(93)90321-2.
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Desmopressin, but not vasopressin, decreases activity of the hypothalamo-neurohypophysial system in Brattleboro rats.去氨加压素而非加压素,可降低布拉特洛维大鼠下丘脑-神经垂体系统的活性。
Regul Pept. 1990 Apr 24;28(2):153-9. doi: 10.1016/0167-0115(90)90014-n.
8
Effects of chemical stimulation of the subfornical organ on metabolic activity of the hypothalamo-neurohypophysial system in rats.穹窿下器化学刺激对大鼠下丘脑-神经垂体系统代谢活性的影响
Neurosci Lett. 1991 Dec 16;134(1):122-6. doi: 10.1016/0304-3940(91)90522-u.
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Role of nitric oxide in the control of luteinizing hormone-releasing hormone release in vivo and in vitro.一氧化氮在体内和体外对促黄体生成激素释放激素释放的调控作用。
Proc Natl Acad Sci U S A. 1993 Nov 1;90(21):10130-4. doi: 10.1073/pnas.90.21.10130.
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Nitric oxide synthase inhibition reduces wakefulness.一氧化氮合酶抑制会降低清醒度。
Neuropharmacology. 1994 Nov;33(11):1505-9. doi: 10.1016/0028-3908(94)90055-8.

引用本文的文献

1
Nitric oxide stimulates ACTH secretion and the transcription of the genes encoding for NGFI-B, corticotropin-releasing factor, corticotropin-releasing factor receptor type 1, and vasopressin in the hypothalamus of the intact rat.一氧化氮可刺激正常大鼠下丘脑促肾上腺皮质激素(ACTH)的分泌以及编码NGFI - B、促肾上腺皮质激素释放因子、1型促肾上腺皮质激素释放因子受体和血管加压素的基因转录。
J Neurosci. 1999 Sep 1;19(17):7640-7. doi: 10.1523/JNEUROSCI.19-17-07640.1999.