Urethane directly inhibits chemoreflex excitation of medullary vasomotor neurons in rats

Miao-Kun Sun, Donald J. Reis
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引用次数: 18

Abstract

In anesthetized rats, stimulation of the arterial chemoreceptors excites reticulospinal vasomotor neurons of the nucleus rostroventrolateral reticularis of the medulla oblongata, via activating the neuronal NMDA receptors. Excitation of these neurons is responsible for reflex increases in sympathetic neuronal activity and arterial pressure. Additional doses (0.12–0.24 g/kg, i.v.) of urethane dose-dependently reduced the elevations in the discharge rate of reticulospinal vasomotor and sympathetic neurons and of arterial pressure, elicited by stimulating the carotid chemoreceptors with intra-carotid injections of sodium cyanide (100 nmol/10 μl), without affecting discharges of the carotid chemoafferents. Microiontophoresis of urethane onto the reticulospinal vasomotor neurons reversibly inhibited the excitation elicited by stimulation of the chemoreceptors and by iontophoretically applied L-glutamate. The results indicate that the suppression of chemoreflexes by excessive amount of urethane is central and one of its actions is blocking excitatory amino acid transmission onto these vasomotor neurons.

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氨基甲酸乙酯直接抑制大鼠髓质血管舒缩神经元的化学反射兴奋
在麻醉大鼠中,动脉化学感受器的刺激通过激活神经元NMDA受体来激活延髓前腹外侧网状核的网状脊髓血管舒缩神经元。这些神经元的兴奋是交感神经元活动和动脉压反射性增加的原因。额外剂量(0.12-0.24 g/kg, i.v)的氨基甲酸乙酯剂量依赖性地降低了颈动脉内注射(100 nmol/10 μl)氰化钠刺激颈动脉化学感受器引起的网状脊髓血管舒缩和交感神经元放电率和动脉压升高,而不影响颈动脉化学传入的放电。氨基甲酸乙酯在网状脊髓血管运动神经元上的微离子电泳可可逆地抑制化学感受器的刺激和离子电泳应用的l -谷氨酸引起的兴奋。结果表明,过量氨基甲酸乙酯对化学反射的抑制是主要的,其作用之一是阻断兴奋性氨基酸向血管舒缩神经元的传递。
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