Kubo T, Kihara M
Arch Int Pharmacodyn Ther. 1987 Feb;285(2):277-87.
Cardiovascular effects of chemical stimulation of the rostral ventrolateral medulla were studied in pentobarbital-anesthetized, paralyzed rats to examine the medullary GABAergic mechanisms responsible for cardiovascular regulation. Bilateral microinjections of 3-mercaptopropionic acid (10 micrograms), an inhibitor of gamma-aminobutyric acid (GABA) synthesis, into the ventrolateral medulla produced an increase in blood pressure and heart rate. Unilateral microinjection of nipecotic acid (3 micrograms), a reuptake inhibitor of GABA, elicited a fall in arterial pressure and heart rate. Bilateral microinjections of bicuculline (100 pmol), a GABA antagonist, into the ventrolateral medulla produced a sustained increase in arterial pressure and heart rate and, in addition, inhibited the hypotensive action induced by veratrine (0.3 mg/kg, i.v.). Lesioning of the rat nucleus tractus solitarii did not alter GABA content in the rostral ventrolateral medulla. These results support the hypothesis that in the rostral ventrolateral medulla, there exist GABAergic mechanisms involved in cardiovascular regulation. It seems unlikely that the GABAergic mechanisms originate mainly from neurons in the nucleus tractus solitarii.
在戊巴比妥麻醉、麻痹的大鼠中研究了延髓头端腹外侧化学刺激的心血管效应，以检验负责心血管调节的延髓GABA能机制。向腹外侧延髓双侧微量注射3-巯基丙酸（10微克），一种γ-氨基丁酸（GABA）合成抑制剂，可使血压和心率升高。向腹外侧延髓单侧微量注射GABA再摄取抑制剂尼克酸（3微克），可引起动脉压和心率下降。向腹外侧延髓双侧微量注射GABA拮抗剂荷包牡丹碱（100皮摩尔），可使动脉压和心率持续升高，此外，还可抑制藜芦碱（0.3毫克/千克，静脉注射）诱导的降压作用。损毁大鼠孤束核并不改变延髓头端腹外侧的GABA含量。这些结果支持这样的假说，即在延髓头端腹外侧存在参与心血管调节的GABA能机制。GABA能机制似乎不太可能主要起源于孤束核中的神经元。
