Ito S, Sved A F
Department of Neuroscience, University of Pittsburgh, Pennsylvania 15260, USA.
Am J Physiol. 1997 Aug;273(2 Pt 2):R487-94. doi: 10.1152/ajpregu.1997.273.2.R487.
Sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) play a key role in the tonic maintenance of resting arterial pressure. Removal of tonically active inhibitory inputs to the RVLM provided by the caudal ventrolateral medulla (CVLM) elicits a large increase in arterial pressure. The present study addresses the hypothesis that excitatory amino acids (EAA) provide the excitation of the RVLM responsible for the increase in arterial pressure that occurs after withdrawal of CVLM-mediated inhibition of the RVLM. In rats anesthetized with either alpha-chloralose or urethan, inhibition of the CVLM by local injection of muscimol markedly elevated arterial pressure. Subsequent injection of the EAA receptor antagonist kynurenic acid into the RVLM caused arterial pressure to fall to levels comparable to those that occur-with total autonomic blockade. In contrast, injection of kynurenic acid into the RVLM of control rats had little effect on arterial pressure. These results indicate that the large increase in arterial pressure produced by inhibition of the CVLM is mediated by EAA excitation of RVLM neurons. Furthermore, these data suggest that EAA play a prominent role in the tonic excitation of RVLM neurons, but, in intact rats, inhibition of EAA in the RVLM elicits no change in arterial pressure because of removal of inhibitory as well as excitatory drives of the RVLM.
延髓头端腹外侧区(RVLM)的交感兴奋性神经元在静息动脉血压的紧张性维持中起关键作用。去除尾端腹外侧区(CVLM)对RVLM的紧张性活动抑制性输入会引起动脉血压大幅升高。本研究探讨了这样一个假说,即兴奋性氨基酸(EAA)对RVLM产生兴奋作用,这与CVLM介导的对RVLM的抑制作用撤除后出现的动脉血压升高有关。在用α-氯醛糖或氨基甲酸乙酯麻醉的大鼠中,通过局部注射蝇蕈醇抑制CVLM可显著升高动脉血压。随后向RVLM注射EAA受体拮抗剂犬尿氨酸会使动脉血压降至与完全自主神经阻滞时相当的水平。相比之下,向对照大鼠的RVLM注射犬尿氨酸对动脉血压几乎没有影响。这些结果表明,抑制CVLM所导致的动脉血压大幅升高是由RVLM神经元的EAA兴奋介导的。此外,这些数据表明EAA在RVLM神经元的紧张性兴奋中起重要作用,但在完整大鼠中,抑制RVLM中的EAA不会引起动脉血压变化,因为同时去除了RVLM的抑制性和兴奋性驱动。