Kobayashi A, Osaka T, Namba Y, Inoue S, Kimura S
Showa Women's University Graduate School, 1-7 Taishido, Setagaya-ku, Tokyo, Japan.
Brain Res. 1999 Dec 4;849(1-2):196-202. doi: 10.1016/s0006-8993(99)02154-x.
We previously reported that microinjection of calcitonin gene-related peptide (CGRP; 1.6-8.0 pmol, 0.2-1.0 microliter) into the ventromedial hypothalamus (VMH) increased oxygen consumption (VO(2)), heart rate (HR), colonic temperature (T(co)), and temperature of interscapular brown adipose tissue (T(IBAT)). In the present study, we investigated whether the autonomic nervous system is involved in the CGRP-induced heat production in urethane-anesthetized rats. Intraperitoneal administration of the ganglion blocker hexamethonium (20 mg/kg) or the beta-adrenergic antagonist propranolol (5 mg/kg) suppressed the CGRP-induced increases in VO(2), HR, T(co), and T(IBAT). Pretreatment with the alpha-adrenergic antagonist phentolamine (5 mg/kg) partly attenuated the heat production response but did not affect the tachycardiac response. Bilateral sectioning of the nerves supplying the IBAT attenuated the CGRP-induced increase in T(IBAT) but not significantly that in VO(2) or T(co). In rats with adrenal demedullation, the effects of CGRP were similar to those in intact rats. These results suggest that the CGRP-induced heat production is mediated by the sympathetic nervous system and, at least in part, by the BAT through the alpha- and beta-adrenoceptors.
我们先前报道，向腹内侧下丘脑（VMH）微量注射降钙素基因相关肽（CGRP；1.6 - 8.0皮摩尔，0.2 - 1.0微升）可增加氧耗（VO₂）、心率（HR）、结肠温度（T(co)）以及肩胛间棕色脂肪组织温度（T(IBAT)）。在本研究中，我们调查了自主神经系统是否参与了氨基甲酸乙酯麻醉大鼠中CGRP诱导的产热过程。腹腔注射神经节阻滞剂六甲铵（20毫克/千克）或β - 肾上腺素能拮抗剂普萘洛尔（5毫克/千克）可抑制CGRP诱导的VO₂、HR、T(co)和T(IBAT)升高。用α - 肾上腺素能拮抗剂酚妥拉明（5毫克/千克）预处理可部分减弱产热反应，但不影响心动过速反应。切断供应IBAT的神经可减弱CGRP诱导的T(IBAT)升高，但对VO₂或T(co)升高的影响不显著。在肾上腺髓质切除的大鼠中，CGRP的作用与完整大鼠相似。这些结果表明，CGRP诱导的产热由交感神经系统介导，且至少部分通过α和β肾上腺素能受体由棕色脂肪组织介导。
