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α2 -肾上腺素能受体和蛋白激酶C在尼古丁诱导牛脑动脉去甲肾上腺素释放增强中的作用。

Involvement of alpha 2-adrenoceptors and protein kinase C on nicotine-induced facilitation of noradrenaline release in bovine cerebral arteries.

作者信息

Sánchez-Merino J A, Marín J, Balfagón G, Ferrer M

机构信息

Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Madrid, Spain.

出版信息

Gen Pharmacol. 1995 Jul;26(4):827-33. doi: 10.1016/0306-3623(94)00259-p.

DOI:10.1016/0306-3623(94)00259-p
PMID:7635258
Abstract
  1. Incubation of bovine cerebral vessels (previously exposed to [3H]-noradrenaline) with nicotine for 30 sec produced a facilitation of the electrically-induced noradrenaline release, which was antagonized by hexamethonium, a blocker of nicotinic receptors. This facilitation was not observed when the incubation time was increased to 20 or 75 min. 2. Rauwolscine, an alpha 2-adrenoceptor blocker, enhanced and phorbol 12, 13-dibutyrate reduced the facilitator effect produced by 30 sec exposure to nicotine. 3. These data suggest: (1) presynaptic nicotinic receptors produce a facilitation of stimulated noradrenaline release; these receptors are easily desensitized by increasing the incubation time with nicotine; (2) protein kinase C and alpha 2-adrenoceptors appear to be involved in this process.
摘要
  1. 将预先暴露于[3H]-去甲肾上腺素的牛脑血管与尼古丁一起孵育30秒,可促进电诱导的去甲肾上腺素释放,这种促进作用可被烟碱受体阻滞剂六甲铵拮抗。当孵育时间增加到20或75分钟时,未观察到这种促进作用。2. α2-肾上腺素受体阻滞剂育亨宾增强了,而佛波酯12,13-二丁酸酯降低了30秒暴露于尼古丁所产生的促进作用。3. 这些数据表明:(1) 突触前烟碱受体可促进刺激后的去甲肾上腺素释放;通过增加与尼古丁的孵育时间,这些受体很容易脱敏;(2) 蛋白激酶C和α2-肾上腺素受体似乎参与了这一过程。

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引用本文的文献

1
Mechanism of nicotine-evoked release of 3H-noradrenaline in human cerebral cortex slices.尼古丁诱发人脑皮质切片中3H-去甲肾上腺素释放的机制。
Br J Pharmacol. 2002 Dec;137(7):1063-70. doi: 10.1038/sj.bjp.0704975.
2
The regulation of neurotransmitter secretion by protein kinase C.蛋白激酶C对神经递质分泌的调节
Mol Neurobiol. 1998 Oct;18(2):125-55. doi: 10.1007/BF02914269.