Busnardo C, Tavares R F, Antunes-Rodrigues J, Corrêa F M A
Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Av. Bandeirantes 3900, 14049 900 Ribeirão Preto, SP, Brazil.
Neuropharmacology. 2007 May;52(6):1378-84. doi: 10.1016/j.neuropharm.2007.01.011. Epub 2007 Feb 4.
We report on the cardiovascular effects of L-glutamate (L-glu) microinjection in the hypothalamic supraoptic nucleus (SON) as well as possible receptor and mechanisms involved. Microinjection of L-glu in 100 nL in the SON caused dose-related pressor and bradycardic responses in unanesthetized rats. Responses were markedly reduced in urethane-anesthetized rats. The response to L-glu 10 nmol was blocked by local pretreatment with 2 nmol of the non-NMDA-receptors antagonist NBQX and not affected by 2 nmol of the selective NMDA-receptor antagonist LY 235959, suggesting that non-NMDA receptors mediate these responses. The pressor and bradycardic response to L-glu was potentiated by intravenous pretreatment with the ganglion blocker pentolinium and was blocked by intravenous pretreatment with the V1-vasopressin receptor antagonist dTyr(CH2)5(Me)AVP, suggesting involvement of circulating vasopressin in this response. Additionally L-glu microinjection into the SON increased plasma vasopressin levels (control: 1.3 +/- 0.2 pg/mL, n = 6; L-glu: 14.7+/-2.3 pg/mL, n=6). In conclusion the results suggest that pressor responses to SON microinjection of L-glu are caused by activation of non-NMDA glutamate receptors and mediated by vasopressin release into systemic circulation.
我们报告了在下丘脑视上核(SON)中微量注射L-谷氨酸(L-glu)的心血管效应以及可能涉及的受体和机制。在未麻醉的大鼠中,向SON微量注射100 nL的L-glu会引起剂量相关的升压和心动过缓反应。在氨基甲酸乙酯麻醉的大鼠中,这些反应明显减弱。对10 nmol L-glu的反应可被局部预先用2 nmol非NMDA受体拮抗剂NBQX阻断,且不受2 nmol选择性NMDA受体拮抗剂LY 235959的影响,这表明非NMDA受体介导了这些反应。L-glu引起的升压和心动过缓反应可被神经节阻滞剂喷托铵静脉预先处理增强,并被V1-血管加压素受体拮抗剂dTyr(CH2)5(Me)AVP静脉预先处理阻断,这表明循环中的血管加压素参与了该反应。此外,向SON微量注射L-glu会增加血浆血管加压素水平(对照组:1.3±0.2 pg/mL,n = 6;L-glu组:14.7±2.3 pg/mL,n = 6)。总之,结果表明,对SON微量注射L-glu的升压反应是由非NMDA谷氨酸受体的激活引起的,并由血管加压素释放到体循环中介导。