Hochstenbach S L, Ciriello J
Department of Physiology, Health Sciences Centre, University of Western Ontario, London, Canada.
Brain Res. 1994 May 2;644(2):233-42. doi: 10.1016/0006-8993(94)91685-3.
The nucleus of the solitary tract (NTS) was systematically explored in the alpha-chloralose-anesthetized rat for sites that elicited changes in mean arterial pressure (MAP) and heart rate (HR) during microinjections (20 nl) of phosphate-buffered saline (PBS; pH 7.2-7.4) or NaCl solutions containing various concentrations of NaCl (104-326 mM). Decreases in MAP (range 7-83 mmHg) and HR (range 10-70 bpm) were consistently elicited from sites in the caudal medial and commissural subnuclei of NTS. Microinjection of PBS or NaCl into other NTS subnuclei or area postrema did not elicit cardiovascular responses. Microinjection of LiCl in PBS elicited cardiovascular responses that were significantly smaller than those elicited by microinjection of NaCl in PBS at the same NTS site. Injections of either a hyperosmotic (400 mOsm/kg) or a hyposmotic (204 mOsm/kg) solution of mannitol into NaCl-sensitive sites did not elicit cardiovascular responses. Finally, most of the sites in NTS that elicited cardiovascular responses during microinjection of glutamate (1 M) did not respond to microinjections of PBS. Administration of atropine methyl bromide had no effect on the magnitude of the depressor response to injections of PBS into NTS, but significantly attenuated (32%) the HR response. Subsequent administration of the ganglionic blockers hexamethonium bromide or arfonad abolished both the depressor and bradycardic responses. These data suggest that within a restricted region of the caudal NTS there exists a pool of neurons sensitive to changes in extracellular Na+ concentrations that, when activated by the sodium, elicit vasodepressor responses as a result of sympathoinhibition and bradycardia as a result of vagal excitation and sympathoinhibition.
在α-氯醛糖麻醉的大鼠中，对孤束核（NTS）进行了系统研究，以探寻在微量注射（20 nl）磷酸盐缓冲盐水（PBS；pH 7.2 - 7.4）或含有不同浓度NaCl（104 - 326 mM）的NaCl溶液时，能引起平均动脉压（MAP）和心率（HR）变化的位点。在NTS尾侧内侧和连合亚核的位点持续引发了MAP（范围7 - 83 mmHg）和HR（范围10 - 70次/分钟）的下降。向NTS的其他亚核或最后区微量注射PBS或NaCl未引发心血管反应。在相同的NTS位点，向PBS中微量注射LiCl引发的心血管反应明显小于向PBS中微量注射NaCl所引发的反应。向NaCl敏感位点注射高渗（400 mOsm/kg）或低渗（204 mOsm/kg）甘露醇溶液未引发心血管反应。最后，在微量注射谷氨酸（1 M）期间引发心血管反应的NTS中的大多数位点，对微量注射PBS无反应。给予甲基溴化阿托品对向NTS注射PBS所引起的降压反应幅度无影响，但显著减弱了（32%）HR反应。随后给予神经节阻滞剂溴化六甲铵或阿方那特可消除降压和心动过缓反应。这些数据表明，在尾侧NTS的一个受限区域内，存在一群对细胞外Na⁺浓度变化敏感的神经元，当被钠激活时，由于交感神经抑制而引发血管舒张降压反应，以及由于迷走神经兴奋和交感神经抑制而引发心动过缓。
