alpha-2-Adrenergic activation of proopiomelanocortin-containing neurons in the arcuate nucleus causes opioid-mediated hypotension and bradycardia.
alpha-2-Adrenergic activation of proopiomelanocortin-containing neurons in the arcuate nucleus causes opioid-mediated hypotension and bradycardia.
复制标题
弓状核中含有原阿黑皮质素的神经元的 α2-肾上腺素能激活会导致阿片类药物介导的低血压和心动过缓。
DOI：
10.1159/000126966
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发表时间：
1996
影响因子：
4.1
通讯作者：
Kunos,G
中科院分区：
文献类型：
--
作者：
Li,SJ;Scanlon,MN;Járai,Z;Varga,K;Gantenberg,NS;Lazar-Wesley,E;Kunos,G
用 α-甲基多巴（200 mg/kg/天，腹膜内注射）治疗大鼠 4 天，可增加中基底层下丘脑中阿片黑皮质素原 (POMC) mRNA 的稳态水平（通过 DNA 过量溶液杂交测量）。腹腔注射育亨宾 2 mg/kg/天平行治疗可以防止这种增加，但腹腔注射纳曲酮 2 mg/kg/天则不能。使用外周血管扩张剂肼屈嗪（2 mg/kg/天）治疗不会影响 POMC mRNA 水平。使用 POMC 的 cRNA 探针进行的原位杂交组织化学表明，在对照和 α-甲基多巴治疗的大鼠中，含有 POMC 的细胞均位于弓状核的范围内，并证实了后者中 POMC mRNA 的增加。将 2 µg α-甲基去甲肾上腺素单侧微量注射到乌拉坦麻醉大鼠的弓状核中会引起低血压和心动过缓，可以通过在同一部位微量注射 200 ng 育亨宾或在同侧孤束核微量注射 100 ngl-纳洛酮来抑制。 但不进入弓状核。这些发现被解释为表明位于弓状核中含有POMC的神经元上的α2-肾上腺素能受体的激活导致β-内啡肽释放并刺激NTS中的阿片受体，从而导致低血压和心动过缓，并且该机制有助于α-甲基多巴的降血压作用。
Treatment of rats for 4 days with α-methyldopa, 200 mg/kg/day i.p., increases steady state levels of proopiomelanocortin (POMC) mRNA in the mediobasal hypothalamus, as measured by DNA excess solution hybridization. The increase is prevented by parallel treatment with yohimbine, 2 mg/kg/day i.p., but not by naltrexone, 2 mg/kg/day i.p. Treatment with the peripheral vasodilator hydralazine, 2 mg/kg/day, does not affect POMC mRNA levels. In situ hybridization histochemistry with a cRNA probe for POMC indicates that POMC-containing cells are located within the confines of the arcuate nucleus both in control and in α-methyldopa-treated rats, and confirms the increase in POMC mRNA in the latter. Microinjection of 2 µg of α-methylnorepinephrine unilaterally into the arcuate nucleus of urethane-anesthetized rats causes hypotension and bradycardia, which can be inhibited by 200 ng of yohimbine microinjected into the same site, or by 100 ngl-naloxone microinjected into the ipsilateral nucleus tractus solitarii, but not into the arcuate nucleus. These findings are interpreted to indicate that activation of α2-adrenergic receptors located on POMC-containing neurons in the arcuate nucleus causes β-endorphin release and stimulation of opiate receptors in the NTS, which results in hypotension and bradycardia, and that this mechanism contributes to the hypotensive action of α-methyldopa.