Natarajan M, Morrison S F
Department of Physiology (M211), Northwestern University Medical School, 303 E. Chicago Avenue, Chicago, IL 60611, USA.
Brain Res. 1999 May 8;827(1-2):169-75. doi: 10.1016/s0006-8993(99)01332-3.
By providing the principal inhibitory regulation of the discharge of sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM), neurons in the caudal ventrolateral medulla (CVLM) play a major role in regulating the level of sympathetic nerve activity (SNA) to cardiovascular targets. To determine whether adrenal medullary secretion of epinephrine (EPI) is also regulated by sympathoinhibitory inputs from the CVLM to the RVLM, we compared levels of plasma EPI obtained after disinhibition of RVLM neurons with levels obtained after inhibition of CVLM neurons, both of which result in sustained elevations in arterial blood pressure (AP), SNA, and heart rate (HR). Plasma norepinephrine (NE) concentrations were significantly elevated following bilateral microinjection either of bicuculline (BIC) into the RVLM or of muscimol into the CVLM of urethane/chloralose-anesthetized, artificially-ventilated rats. In sharp contrast, although plasma EPI concentrations were significantly elevated following disinhibition of neurons in the RVLM, they were unchanged by inhibition of neurons in the CVLM. These results demonstrate that the discharge of sympathetic premotor neurons in the RVLM regulating adrenal secretion of EPI is modulated by a tonic, GABA-ergic inhibition that arises from a source that is different from the sympathoinhibitory neurons in the CVLM that project to RVLM sympathetic premotor neurons controlling vasoconstrictor and cardiac targets.
通过对延髓头端腹外侧区（RVLM）交感神经运动前神经元的放电提供主要的抑制性调节，延髓尾端腹外侧区（CVLM）的神经元在调节对心血管靶标的交感神经活动（SNA）水平中起主要作用。为了确定肾上腺髓质肾上腺素（EPI）的分泌是否也受从CVLM到RVLM的交感抑制性输入的调节，我们比较了RVLM神经元去抑制后获得的血浆EPI水平与CVLM神经元抑制后获得的血浆EPI水平，这两种情况都会导致动脉血压（AP）、SNA和心率（HR）持续升高。在对氨基甲酸乙酯/氯醛糖麻醉、人工通气的大鼠双侧微量注射荷包牡丹碱（BIC）到RVLM或注射蝇蕈醇到CVLM后，血浆去甲肾上腺素（NE）浓度显著升高。与之形成鲜明对比的是，虽然RVLM神经元去抑制后血浆EPI浓度显著升高，但CVLM神经元抑制后血浆EPI浓度却没有变化。这些结果表明，调节肾上腺EPI分泌的RVLM交感神经运动前神经元的放电受到一种持续性的、γ-氨基丁酸能抑制的调节，这种抑制源于一个不同于投射到控制血管收缩和心脏靶标的RVLM交感神经运动前神经元的CVLM交感抑制性神经元的来源。
