Sympathetic and parasympathetic component of bradycardia triggered by stimulation of NTS P2X receptors.
Sympathetic and parasympathetic component of bradycardia triggered by stimulation of NTS P2X receptors.
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由 NTS P2X 受体刺激引发的心动过缓的交感神经和副交感神经成分。
DOI：
10.1152/ajpheart.00889.2005
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Scislo,TadeuszJ
中科院分区：
文献类型：
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作者：
Kitchen,AmyM;O'Leary,DonalS;Scislo,TadeuszJ
我们之前已经证明，孤束后核 (NTS) 中 P2X 嘌呤受体的激活会导致快速心动过缓和低血压。这种心动过缓可能通过交感神经退缩、副交感神经激活或两种机制的组合而发生。因此，我们研究了副交感神经激活和交感神经撤退在介导氯醛糖-氨基甲酸乙酯麻醉的雄性斯普拉格-道利大鼠心动过缓中的相对作用。将选择性 P2X 嘌呤受体激动剂 α,β-亚甲基 ATP（25 pmol/50 nl 和 100 pmol/50 nl）显微注射到对照动物的皮下 NTS 中，然后注射阿替洛尔（2 mg/kg iv）（一种 β1 选择性拮抗剂）和阿托品甲基溴（2 mg/kg iv）（一种毒蕈碱受体拮抗剂）。在低剂量激动剂激活 P2X 受体时观察到的心动过缓几乎完全是由交感神经退缩介导的。 β1-肾上腺素能阻断后，心动过缓降至仅-5.1±0.5次/分钟，而完整动物中为-28.8±5.1次/分钟。在低剂量下，毒蕈碱阻断不会对心动过缓反应产生任何显着变化。在高剂量下，β1-肾上腺素能阻断和毒蕈碱阻断均类似地减弱心动过缓，分别为-37.4±6.4和-40.6±3.7次/分钟，而对照组动物为-88.0±11次/分钟。 β1-肾上腺素能受体和毒蕈碱受体的双重阻断实际上消除了反应（−2.5 ± 0.8 次/分钟）。我们得出的结论是，副交感神经激活和交感神经撤退的相对贡献取决于 P2X 受体激活的程度。
We have previously shown that activation of P2X purinoceptors in the subpostremal nucleus tractus solitarius (NTS) produces a rapid bradycardia and hypotension. This bradycardia could occur via sympathetic withdrawal, parasympathetic activation, or a combination of both mechanisms. Thus we investigated the relative roles of parasympathetic activation and sympathetic withdrawal in mediating this bradycardia in chloralose-urethane anesthetized male Sprague-Dawley rats. Microinjections of the selective P2X purinoceptor agonist α,β-methylene ATP (25 pmol/50 nl and 100 pmol/50 nl) were made into the subpostremal NTS in control animals, after atenolol (2 mg/kg iv), a β1-selective antagonist, and after atropine methyl bromide (2 mg/kg iv), a muscarinic receptor antagonist. The bradycardia observed with activation of P2X receptors at the low dose of the agonist is mediated almost entirely by sympathetic withdrawal. After β1-adrenergic blockade, the bradycardia was reduced to just −5.1 ± 0.5 versus −28.8 ± 5.1 beats/min in intact animals. Muscarinic blockade did not produce any significant change in the bradycardic response at the low dose. At the high dose, both β1-adrenergic blockade and muscarinic blockade attenuated the bradycardia similarly, −37.4 ± 6.4 and −40.6 ± 3.7 beats/min, respectively, compared with −88.0 ± 11 beats/min in control animals. Double blockade of both β1-adrenergic and muscarinic receptors virtually abolished the response (−2.5 ± 0.8 beats/min). We conclude that the relative contributions of parasympathetic activation and sympathetic withdrawal are dependent on the extent of P2X receptor activation.