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Br J Pharmacol. 1994 Dec;113(4):1358-62. doi: 10.1111/j.1476-5381.1994.tb17147.x.
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本文引用的文献

1
A proposed new nomenclature for 5-HT receptors.一种关于5-羟色胺受体的新命名提议。
Trends Pharmacol Sci. 1993 Jun;14(6):233-6. doi: 10.1016/0165-6147(93)90016-d.
2
5-hydroxytryptamine and vascular disease.5-羟色胺与血管疾病
Fed Proc. 1983 Feb;42(2):233-7.
3
The effect of bilateral adrenal demedullation on vascular reactivity and blood pressure in spontaneously hypertensive rats.双侧肾上腺髓质剥除术对自发性高血压大鼠血管反应性和血压的影响。
Br J Pharmacol. 1983 Nov;80(3):429-37. doi: 10.1111/j.1476-5381.1983.tb10712.x.
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Neuronal 5-HT receptors in the periphery.外周的神经元5-羟色胺受体。
Neuropharmacology. 1984 Dec;23(12B):1473-86. doi: 10.1016/0028-3908(84)90091-1.
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Serotonin enhances sympathetic vasoconstrictor responses in rat isolated perfused tail artery by activation of postjunctional serotonin-2 receptors.血清素通过激活节后血清素-2受体增强大鼠离体灌注尾动脉的交感缩血管反应。
Clin Exp Pharmacol Physiol. 1984 Jul-Aug;11(4):343-6. doi: 10.1111/j.1440-1681.1984.tb00275.x.
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Antihypertensive effects of chronic 5-hydroxytryptamine (5-HT2) receptor blockade with ketanserin in the spontaneously hypertensive rat.酮色林对自发性高血压大鼠慢性5-羟色胺(5-HT2)受体阻滞的降压作用
Naunyn Schmiedebergs Arch Pharmacol. 1984 Aug;327(1):43-7. doi: 10.1007/BF00504990.
7
MDL 72222: a potent and highly selective antagonist at neuronal 5-hydroxytryptamine receptors.MDL 72222:一种强效且高度选择性的神经元5-羟色胺受体拮抗剂。
Naunyn Schmiedebergs Arch Pharmacol. 1984 May;326(1):36-44. doi: 10.1007/BF00518776.
8
Evidence for a presynaptic inhibitory action of 5-hydroxytryptamine on sympathetic neurotransmission to the myocardium.5-羟色胺对交感神经向心肌神经传递的突触前抑制作用的证据。
Eur J Pharmacol. 1980 May 16;63(4):303-11. doi: 10.1016/0014-2999(80)90259-9.
9
Effect of desipramine on the effects of alpha-adrenoceptor inhibitors on pressor responses and release of norepinephrine into plasma of pithed rats.
J Cardiovasc Pharmacol. 1983 Mar-Apr;5(2):297-301. doi: 10.1097/00005344-198303000-00022.
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An analysis of the mechanism of 5-hydroxytryptamine-induced vasopressor responses in ganglion-blocked anaesthetized dogs.
J Pharm Pharmacol. 1981 Mar;33(3):155-60. doi: 10.1111/j.2042-7158.1981.tb13739.x.

抑制性5-羟色胺受体参与在脊髓横断大鼠中通过刺激脊髓交感神经传出而获得的升压效应。

Inhibitory 5-hydroxytryptamine receptors involved in pressor effects obtained by stimulation of sympathetic outflow from spinal cord in pithed rats.

作者信息

Morán A, Velasco C, Salvador T, Martín M L, San Román L

机构信息

Departamento de Fisiología y Farmacología, Facultad de Farmacia, Universidad de Salamanca, Spain.

出版信息

Br J Pharmacol. 1994 Dec;113(4):1358-62. doi: 10.1111/j.1476-5381.1994.tb17147.x.

DOI:10.1111/j.1476-5381.1994.tb17147.x
PMID:7889292
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1510480/
Abstract
  1. A study was made of the effects of 5-hydroxytryptamine (5-HT) on pressor response induced in vivo by electrical stimulation of the sympathetic outflow from the spinal cord of pithed rats. All animals had been pretreated with atropine. Intravenous infusion of 5-hydroxytryptamine at doses of 10 and 20 micrograms kg-1 min-1 reduced the pressor effects obtained by electrical stimulation at intervals of 10 min over the 1 h of infusion. 2. This inhibitory action of 5-HT was depressed by cyproheptadine and methiothepin but was not modified by ketanserin or MDL-72222. By contrast, the inhibitory action of 5-HT was lost in pithed rats that had been pretreated with exogenous noradrenaline. 3. The 5-HT1 receptor agonist 5-carboxamidotryptamine (5-CT) caused an inhibition of the pressor response, whereas the 5-HT3 receptor agonist, 1-phenylbiguanide, produced a variable but significant increase in the pressor response. The 5-HT2 receptor agonist, m-CPP, did not modify the pressor sympathetic response. 4. Our results suggest that 5-hydroxytryptamine interferes with sympathetic neurotransmission by inhibiting pressor effects as a result of stimulation of the complete sympathetic outflow, and that this inhibition is mainly through a presynaptic 5-HT1 mechanism.
摘要
  1. 本研究旨在探讨5-羟色胺(5-HT)对脊髓切断大鼠脊髓交感神经传出纤维电刺激诱导的体内升压反应的影响。所有动物均预先用阿托品处理。静脉输注剂量为10和20微克/千克·分钟的5-羟色胺,在输注1小时内,每隔10分钟降低电刺激所获得的升压效应。2. 5-HT的这种抑制作用被赛庚啶和甲硫噻平所抑制,但未被酮色林或MDL-72222所改变。相比之下,预先用外源性去甲肾上腺素处理的脊髓切断大鼠中,5-HT的抑制作用消失。3. 5-HT1受体激动剂5-羧酰胺色胺(5-CT)引起升压反应的抑制,而5-HT3受体激动剂1-苯基双胍则使升压反应产生可变但显著的增加。5-HT2受体激动剂间氯苯哌嗪未改变交感神经升压反应。4. 我们的结果表明,5-羟色胺通过抑制完全交感神经传出纤维刺激所产生的升压效应来干扰交感神经传递,并且这种抑制主要通过突触前5-HT1机制。