Saito H, Thapaliya S, Matsuyama H, Nishimura M, Takewaki T
Department of Pathogenetic Veterinary Science, United Graduate School, Gifu University, Yanagido 1-1, Gifu city, 501-1193, Japan.
J Physiol. 2001 Mar 1;531(Pt 2):495-507. doi: 10.1111/j.1469-7793.2001.0495i.x.
The present study investigated the effects of hibernation and hibernating body temperature (10 degrees C) on the relative changes that may occur in adrenergic and purinergic perivascular neurotransmission of the golden hamster. The hindlimb resistance vessels and the tibial artery of age-matched controls, cold exposed controls and hibernated hamsters were examined by pharmacological and electrophysiological techniques. At 34 degrees C, electrical field stimulation (EFS; supramaximal voltage, 0.5 ms; for 10 s) in all three groups evoked only twitch responses at 1-5 Hz, which were inhibited by piridoxal phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), a 2PX receptor antagonist. At 10-50 Hz the twitch responses were followed by sustained contractile responses, which were inhibited by prazosin, an alpha1-adrenoceptor antagonist. These responses were markedly enhanced at higher frequencies in hibernated tissues. At 10 degrees C, EFS evoked only the PPADS-sensitive transient responses in all the three groups, and this was markedly enhanced in hibernated tissues. At 34 degrees C, a single stimulus evoked a PPADS-sensitive excitatory junction potential (EJP) in all three groups but a train of pulses (e.g. approximately 0.5) evoked EJPs and prazosin-sensitive sustained depolarizations. These responses were markedly enhanced in hibernated cells. At 10 degrees C, either a single stimulus or a train of stimuli evoked only transient PPADS-sensitive EJPs, which were markedly enhanced in hibernated cells. The contractile responses and electrical membrane responses to exogenous ATP (1-1000 microM) and noradrenaline (0.1-100 microM) were unchanged in the three groups at 34 and at 10 degrees C. These results suggest that during hibernation enhancement of ATP release from the sympathetic perivascular nerves may occur, leading to an efficient means for maintenance of vascular tone and peripheral resistance.
本研究调查了冬眠及冬眠体温(10摄氏度)对金黄仓鼠肾上腺素能和嘌呤能血管周围神经传递可能发生的相对变化的影响。采用药理学和电生理学技术,对年龄匹配的对照组、冷暴露对照组和冬眠仓鼠的后肢阻力血管及胫动脉进行了检测。在34摄氏度时,三组的电场刺激(EFS;超最大电压,0.5毫秒;持续10秒)仅在1 - 5赫兹时诱发抽搐反应,该反应被2PX受体拮抗剂磷酸吡哆醛 - 6 - 偶氮苯 - 2',4'-二磺酸(PPADS)抑制。在10 - 50赫兹时,抽搐反应后跟随持续收缩反应,该反应被α1肾上腺素能受体拮抗剂哌唑嗪抑制。这些反应在冬眠组织的较高频率下显著增强。在10摄氏度时,EFS在三组中仅诱发PPADS敏感的瞬时反应,且在冬眠组织中显著增强。在34摄氏度时,单次刺激在三组中均诱发PPADS敏感的兴奋性接头电位(EJP),但一串脉冲(如约0.5)诱发EJP和哌唑嗪敏感的持续去极化。这些反应在冬眠细胞中显著增强。在10摄氏度时,单次刺激或一串刺激仅诱发瞬时的PPADS敏感EJP,且在冬眠细胞中显著增强。在34摄氏度和10摄氏度时,三组对外源性ATP(1 - 1000微摩尔)和去甲肾上腺素(0.1 - 100微摩尔)的收缩反应和电膜反应均未改变。这些结果表明,在冬眠期间,交感神经血管周围神经的ATP释放可能增强,从而形成维持血管张力和外周阻力的有效方式。