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首页> 外文期刊>American Journal of Physiology >Adrenomedullin in the rostral ventrolateral medulla increases arterial pressure and heart rate: roles of glutamate and nitric oxide.
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Adrenomedullin in the rostral ventrolateral medulla increases arterial pressure and heart rate: roles of glutamate and nitric oxide.

机译：延髓腹侧延髓中的肾上腺髓质素增加动脉压和心率：谷氨酸和一氧化氮的作用。

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摘要

This study was done to investigate the effects of microinjections of adrenomedullin (ADM), a vasoactive neuropeptide, in the rostral ventrolateral medulla (RVLM) on mean arterial pressure (MAP) and heart rate (HR) in urethane-anesthetized rats, and to assess the potential roles of glutamate and nitric oxide (NO) in these effects. Unilateral injections of ADM (0.01 or 0.1 pmol) into the RVLM significantly increased MAP and HR in a dose-dependent manner, whereas ADM at 0.001 pmol was ineffective. Microinjections of ADM (0.01 pmol) outside the RVLM had no effects on MAP or HR. Coinjections of a putative ADM receptor antagonist, ADM(22-52) (0.01 pmol), abolished the increases in MAP and HR evoked by ADM (0.01 pmol). The vasopressor effects of ADM (0.01 pmol) in the RVLM were abolished by coinjections of either dizocilpine hydrogen maleate (a selective NMDA glutamate receptor antagonist, 500 pmol) or 6-cyano-7-nitroquinoxaline-2,3-dione (a selective non-NMDA glutamate receptor antagonist, 50 pmol). The ADM-induced vasopressor effects were also abolished by coadministration of either 7-nitroindazole sodium salt (a selective neuronal NO synthase inhibitor, 0.05 pmol) or methylene blue (a soluble guanylyl cyclase inhibitor, 100 pmol). These results suggest that ADM in the RVLM stimulates increases in MAP and HR through ADM receptor-mediated mechanisms. These effects are mediated by glutamate via both NMDA and non-NMDA receptors. NO, derived from neuronal NO synthase, also contributes to the ADM-induced vasopressor effects via a soluble guanylyl cyclase-associated signaling pathway.
机译：这项研究的目的是研究经尿烷麻醉的大鼠的腹侧延髓延髓（RVLM）微注射肾上腺髓质素（ADM），血管活性神经肽对平均动脉压（MAP）和心率（HR）的影响，并评估谷氨酸和一氧化氮（NO）在这些效应中的潜在作用。向RVLM单侧注射ADM（0.01或0.1 pmol）会以剂量依赖性方式显着增加MAP和HR，而0.001 pmol的ADM无效。 RVLM外部微量注射ADM（0.01 pmol）对MAP或HR无影响。推定的ADM受体拮抗剂ADM（22-52）（0.01 pmol）的共同注射消除了ADM（0.01 pmol）引起的MAP和HR升高。通过同时注射马来酸地佐西平（选择性NMDA谷氨酸受体拮抗剂500 pmol）或6-氰基-7-硝基喹喔啉-2,3-二酮（一种选择性非-NMDA谷氨酸受体拮抗剂（50 pmol）。通过同时使用7-硝基吲唑钠盐（选择性神经元NO合酶抑制剂，0.05 pmol）或亚甲基蓝（可溶性鸟苷酸环化酶抑制剂，100 pmol），也消除了ADM诱导的血管升压作用。这些结果表明，RVLM中的ADM通过ADM受体介导的机制刺激MAP和HR升高。这些作用是由谷氨酸通过NMDA和非NMDA受体介导的。来源于神经元一氧化氮合酶的一氧化氮也通过可溶性鸟苷酸环化酶相关的信号传导途径促进了ADM诱导的血管升压作用。

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