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交感神经激活增加正常血压大鼠而非高血压大鼠基底动脉血流。

Sympathetic activation increases basilar arterial blood flow in normotensive but not hypertensive rats.

机构信息

Institute of Medical Sciences, College of Medicine, Tzu Chi University, Hualien, Taiwan.

出版信息

Am J Physiol Heart Circ Physiol. 2012 Mar 1;302(5):H1123-30. doi: 10.1152/ajpheart.01016.2011. Epub 2011 Dec 30.

Abstract

The close apposition between sympathetic and parasympathetic nerve terminals in the adventitia of cerebral arteries provides morphological evidence that sympathetic nerve activation causes parasympathetic nitrergic vasodilation via a sympathetic-parasympathetic interaction mechanism. The decreased parasympathetic nerve terminals in basilar arteries (BA) of spontaneously hypertensive rat (SHR) and renovascular hypertensive rats (RHR) compared with Wistar-Kyoto rats (WKY), therefore, would diminish this axo-axonal interaction-mediated neurogenic vasodilation in hypertension. Increased basilar arterial blood flow (BABF) via axo-axonal interaction during sympathetic activation was, therefore, examined in anesthetized rats by laser-Doppler flowmetry. Electrical stimulation (ES) of sympathetic nerves originating in superior cervical ganglion (SCG) and topical nicotine (10-30 μM) onto BA of WKY significantly increased BABF. Both increases were inhibited by tetrodotoxin, 7-nitroindazole (neuronal nitric oxide synthase inhibitor), and ICI-118,551 (β(2)-adrenoceptor antagonist), but not by atenolol (β(1)-adrenoceptor antagonist). Topical norepinephrine onto BA also increased BABF, which was abolished by atenolol combined with 7-nitroindazole or ICI-118,551. Similar results were found in prehypertensive SHR. However, in adult SHR and RHR, ES of sympathetic nerves or topical nicotine caused minimum or no increase of BABF. It is concluded that excitation of sympathetic nerves to BA in WKY causes parasympathetic nitrergic vasodilation with increased BABF. This finding indicates an endowed functional neurogenic mechanism for increasing the BABF or brain stem blood flow in coping with increased local sympathetic activities in acutely stressful situations such as the "fight-or-flight response." This increased blood flow in defensive mechanism diminishes in genetic and nongenetic hypertensive rats due most likely to decreased parasympathetic nitrergic nerve terminals.

摘要

大脑动脉外膜中交感和副交感神经末梢的紧密毗邻提供了形态学证据,表明交感神经激活通过交感-副交感相互作用机制引起副交感神经 nitrergic 血管舒张。与 Wistar-Kyoto 大鼠 (WKY) 相比,自发性高血压大鼠 (SHR) 和肾血管性高血压大鼠 (RHR) 的基底动脉 (BA) 中的副交感神经末梢减少,因此会减少高血压中这种轴突-轴突相互作用介导的神经源性血管舒张。因此,通过激光多普勒流量测定法在麻醉大鼠中检查交感神经激活期间通过轴突-轴突相互作用增加的基底动脉血流 (BABF)。来自颈上神经节 (SCG) 的交感神经的电刺激 (ES) 和 BA 上的尼古丁 (10-30 μM) 显著增加了 BABF。这两种增加均被河豚毒素、7-硝基吲唑 (神经元一氧化氮合酶抑制剂) 和 ICI-118,551 (β2-肾上腺素能受体拮抗剂) 抑制,但不被阿替洛尔 (β1-肾上腺素能受体拮抗剂) 抑制。BA 上的去甲肾上腺素也增加了 BABF,阿替洛尔与 7-硝基吲唑或 ICI-118,551 联合使用可消除该增加。在预高血压 SHR 中也发现了类似的结果。然而,在成年 SHR 和 RHR 中,交感神经 ES 或尼古丁对 BA 的局部应用仅引起最小或无 BABF 增加。结论是,WKY 中 BA 的交感神经兴奋引起副交感神经 nitrergic 血管舒张,并增加 BABF。这一发现表明,在急性应激情况下(如“战斗或逃跑反应”),存在一种赋予的功能性神经源性机制,用于增加 BABF 或脑干血流量,以应对局部交感神经活动的增加。这种防御机制中的增加的血流量在遗传和非遗传高血压大鼠中减少,这很可能是由于副交感神经 nitrergic 神经末梢减少所致。

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