Machado Benedito H, Bonagamba Leni G H
Department Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, 14049-900, Ribeirão Preto, SP, Brazil.
Auton Neurosci. 2005 Jan 15;117(1):25-32. doi: 10.1016/j.autneu.2004.10.004.
The role of excitatory amino acid (EAA) receptors in the neurotransmission of the sympathoexcitatory component of the chemoreflex (pressor response) in the intermediate and caudal aspects of the commissural nucleus tractus solitarii (NTS) of awake rats was evaluated. Microinjection of kynurenic acid, a non-selective antagonist of EAA receptors, into the intermediate and caudal commissural NTS produced a large increase in the baseline mean arterial pressure (MAP), which may reduce the magnitude of the pressor response to chemoreflex activation. To avoid this problem sodium nitroprusside (SNP) was infused (i.v.) after microinjections of kynurenic acid (2 nmol/50 nl) into the NTS, in order to normalize the MAP and then the chemoreflex was activated and the magnitude of the pressor response evaluated. Microinjection of kynurenic acid into the intermediate (bilaterally) and caudal (midline) commissural NTS (n=6) produced a significant increase in baseline MAP (103+/-5 vs. 137+/-6 mm Hg) normalized by SNP infusion (107+/-4 mm Hg) and under this experimental condition the pressor response to chemoreflex activation was not statistically different in relation to the control (37+/-7 vs. 44+/-6 mm Hg). Bilateral microinjections of kynurenic acid into the caudal NTS (n=8) also produced a significant increase in baseline MAP (109+/-4 vs. 145+/-6 mm Hg) normalized by SNP infusion (109+/-6 mm Hg). After normalization of MAP, the pressor response to chemoreflex activation at 3 (34+/-6 mm Hg) and 10 min (37+/-6 mm Hg) was also not different in relation to the control (46+/-5 mm Hg). These data indicate that the antagonism of EAA receptors simultaneously in the intermediate (bilateral) and caudal (midline) commissural NTS or only in the caudal commissural NTS (bilateral) of awake rats had no effect on the hypertensive response to chemoreflex activation. We suggest that neurotransmitter other than l-glutamate may take part in the neurotransmission of the sympathoexcitatory component of the chemoreflex at the NTS level.
评估了兴奋性氨基酸（EAA）受体在清醒大鼠孤束核（NTS）中间和尾部化学反射（升压反应）的交感兴奋成分神经传递中的作用。向中间和尾部联合NTS微量注射犬尿氨酸（一种EAA受体的非选择性拮抗剂），可使基线平均动脉压（MAP）大幅升高，这可能会降低对化学反射激活的升压反应幅度。为避免此问题，在向NTS微量注射犬尿氨酸（2 nmol/50 nl）后静脉输注硝普钠（SNP），以使MAP正常化，然后激活化学反射并评估升压反应幅度。向中间（双侧）和尾部（中线）联合NTS（n = 6）微量注射犬尿氨酸，经SNP输注（107±4 mmHg）使基线MAP显著升高（103±5 vs. 137±6 mmHg），在此实验条件下，对化学反射激活的升压反应与对照组相比无统计学差异（37±7 vs. 44±6 mmHg）。向尾部NTS双侧微量注射犬尿氨酸（n = 8）也使经SNP输注（109±6 mmHg）正常化的基线MAP显著升高（109±4 vs. 145±6 mmHg）。MAP正常化后，在3分钟（34±6 mmHg）和10分钟（37±6 mmHg）时对化学反射激活的升压反应与对照组（46±5 mmHg）相比也无差异。这些数据表明，在清醒大鼠的中间（双侧）和尾部（中线）联合NTS或仅在尾部联合NTS（双侧）同时拮抗EAA受体，对化学反射激活的高血压反应无影响。我们认为，除L-谷氨酸外的神经递质可能参与了NTS水平化学反射交感兴奋成分的神经传递。
