Kubo T, Asari T, Amano M, Hagiwara Y, Fukumori R
Department of Pharmacology, Showa College of Pharmaceutical Sciences, Machida, Tokyo, Japan.
Neurosci Lett. 1997 Aug 29;232(2):103-6. doi: 10.1016/s0304-3940(97)00584-3.
2-Amino-5-phosphonovalerate (AP5; 153 pmol) injected into the rostral ventrolateral medulla (RVLM) inhibited pressor responses induced by carotid chemoreceptor stimulation. AP5 also inhibited pressor responses to aspartate (0.75 nmol) but not to glutamate (0.53 nmol) similarly injected. High K+ (50 mM) released endogenous aspartate and glutamate in a Ca2+-dependent manner from the RVLM. Chemoreceptor stimulation caused a release of aspartate but not of glutamate in the RVLM, and sinus nerve denervation abolished the release of aspartate. Increases in blood pressure induced by intravenous phenylephrine did not release aspartate. These results support the hypothesis that endogenous aspartate in the rat RVLM is involved in the mediation of chemoreceptor reflexes.
注射到延髓头端腹外侧区(RVLM)的2-氨基-5-磷酸戊酸(AP5;153皮摩尔)抑制了颈动脉化学感受器刺激所诱发的升压反应。AP5同样抑制了对类似注射的天冬氨酸(0.75纳摩尔)的升压反应,但对谷氨酸(0.53纳摩尔)的升压反应无抑制作用。高钾(50毫摩尔)以钙依赖的方式从RVLM释放内源性天冬氨酸和谷氨酸。化学感受器刺激导致RVLM中天冬氨酸的释放,但谷氨酸未释放,并且窦神经去神经支配消除了天冬氨酸的释放。静脉注射去氧肾上腺素所诱发的血压升高并未释放天冬氨酸。这些结果支持了大鼠RVLM中的内源性天冬氨酸参与化学感受器反射介导的假说。