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人牙髓中交感神经去甲肾上腺素释放的突触前β-肾上腺素能受体调节

Modulation by presynaptic beta-adrenoceptors of noradrenaline release from sympathetic nerves in human dental pulp.

作者信息

Parker D A, Marino V, Ivar P M, de la Lande I S

机构信息

Department of Dentistry, The University of Adelaide, South Australia.

出版信息

Arch Oral Biol. 1998 Dec;43(12):949-54. doi: 10.1016/s0003-9969(98)00087-9.

Abstract

This study was undertaken to test for the presence of presynaptic beta-adrenoceptors on sympathetic nerves in human dental pulp and, if present, to investigate the subtype. Pulp was excised from freshly extracted teeth, incubated with [3H]-noradrenaline (0.6 micromol/l) and subsequently superfused with Krebs solution. Sympathetic nerves were stimulated at 5 Hz for 100 sec. The non-specific beta-adrenoceptor agonist isoprenaline (1.0 micromol/l), and the selective beta2-agonist salbutamol (10 micromol/l) facilitated the release of [3H]-noradrenaline; isoprenaline, but not salbutamol, also facilitated this release in the presence of desipramine (DMI, 0.3 micromol/l), corticosterone (10 micromol/l) and rauwolscine (0.1 micromol/l). BRL 37344 (1.0 micromol/l), a beta3-agonist, had no effect on [3H]-noradrenaline release. The facilitatory effects of isoprenaline and salbutamol were inhibited by the non-specific beta-antagonist propranolol (1.0 micromol/l), while that of salbutamol was inhibited in the presence of ICI-188,551 (1.0 micromol/l), a selective beta2-antagonist, as well. The beta1-antagonist atenolol (1.0 micromol/l) potentiated the facilitatory effects of isoprenaline in the presence of DMI and corticosterone. Neither propranolol nor ICI-188,551 alone affected the release of [3H]-noradrenaline. These results establish the presence of presynaptic beta-adrenoceptors on sympathetic nerves in human dental pulp. It is suggested that they are of the beta2-subtype, although a greater range of agonists and antagonists needs to be used to clarify the nature of the the beta-adrenoceptors.

摘要

本研究旨在检测人牙髓交感神经上是否存在突触前β-肾上腺素能受体,若存在,则对其亚型进行研究。从新鲜拔除的牙齿中取出牙髓,与[3H]-去甲肾上腺素(0.6微摩尔/升)一起孵育,随后用 Krebs 溶液进行灌流。以5赫兹的频率刺激交感神经100秒。非特异性β-肾上腺素能受体激动剂异丙肾上腺素(1.0微摩尔/升)和选择性β2-激动剂沙丁胺醇(10微摩尔/升)促进了[3H]-去甲肾上腺素的释放;在存在地昔帕明(DMI,0.3微摩尔/升)、皮质酮(10微摩尔/升)和育亨宾(0.1微摩尔/升)的情况下,异丙肾上腺素而非沙丁胺醇也促进了这种释放。β3-激动剂 BRL 37344(1.0微摩尔/升)对[3H]-去甲肾上腺素的释放没有影响。异丙肾上腺素和沙丁胺醇的促进作用被非特异性β-拮抗剂普萘洛尔(1.0微摩尔/升)抑制,而沙丁胺醇的促进作用在存在选择性β2-拮抗剂 ICI-188,551(1.0微摩尔/升)时也被抑制。β1-拮抗剂阿替洛尔(1.0微摩尔/升)在存在 DMI 和皮质酮的情况下增强了异丙肾上腺素的促进作用。单独使用普萘洛尔或 ICI-

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