Department of Medicine, University of Kentucky and VA Medical Center, Lexington, Kentucky 40536, USA.
J Neuroendocrinol. 1990 Jun 1;2(3):381-8. doi: 10.1111/j.1365-2826.1990.tb00422.x.
Abstract The contribution of the adrenal medulla and/or the sympathetic nerves to the plasma levels of Met-enkephalin was investigated. Rats were divided into four groups: sham-operated/saline, sham-operated/guanethidine, adrenal-demedullated/saline, demedulla-ted/guanethidine. After 4 weeks of injection with either saline or guanethidine (25 mg/kg/day), animals were cannulated in the left carotid artery for blood sampling. Three days later, blood samples were taken before and at 2 and 30 min of restraint stress. Adrenal demedullation lowered basal plasma epinephrine levels markedly and prevented entirely the increase induced by restraint stress. Chronic guanethidine treatment lowered basal plasma norepinephrine levels and decreased the response to stress. Guanethidine treatment increased the basal plasma epinephrine level without affecting the response to stress. The combination of guanethidine plus adrenal demedullation lowered basal plasma concentrations of all three catecholamines and further attenuated the norepinephrine response. Restraint stress increased plasma native and peptidase-derivable Met-enkephalin. Adrenal demedullation, resulting in greater than 95% depletion of adrenal catecholamines and significant depletion of adrenal Met-enkephalin, did not inhibit the stress-induced increase in plasma Met-enkephalin, and in fact, was associated with a potentiated response to stress. Guanethidine treatment with or without demedullation increased baseline plasma native Met-enkephalin and abolished the stress-induced increase in plasma native and peptidase-derivable Met-enkephalin. Thus, the stress-induced increase in plasma Metenkephalin results from release from sympathetic nerves, rather than adrenal medulla. However, the sympathetic nerves and adrenal medulla together do not appear to account entirely for basal concentrations of circulating Met-enkephalin. Hepatic portal vein plasma concentration of native Met-enkephalin was greater than that in the carotid artery, suggesting contribution from the gastrointestinal tract; however, evisceration did not decrease plasma native Met-enkephalin. Some compensatory mechanism results in elevation of basal plasma native Met-enkephalin in sympathectomized rats. Also, in the absence of the adrenal medulla there is a compensatory increase in the amount of Met-enkephalin released into the circulation in response to stress.
摘要 本研究旨在探讨肾上腺髓质和/或交感神经对血浆 Met-enkephalin 水平的影响。将大鼠分为四组：假手术/生理盐水组、假手术/胍乙啶组、去肾上腺髓质/生理盐水组和去肾上腺髓质/胍乙啶组。经过 4 周的生理盐水或胍乙啶（25mg/kg/天）注射后，动物通过左侧颈动脉插管进行采血。3 天后，在束缚应激前和 2 分钟及 30 分钟时采集血样。去肾上腺髓质显著降低基础血浆肾上腺素水平，并完全阻止束缚应激引起的增加。慢性胍乙啶处理降低基础血浆去甲肾上腺素水平，并减少应激反应。胍乙啶处理增加基础血浆肾上腺素水平而不影响应激反应。胍乙啶加去肾上腺髓质联合处理降低基础血浆中所有三种儿茶酚胺的浓度，并进一步减弱去甲肾上腺素的反应。束缚应激增加了血浆中天然和肽酶衍生的 Met-enkephalin。去肾上腺髓质导致肾上腺儿茶酚胺耗竭超过 95%，并显著耗竭肾上腺 Met-enkephalin，但不抑制应激引起的血浆 Met-enkephalin 增加，实际上与应激反应增强有关。胍乙啶处理，无论是否去肾上腺髓质，均增加基础血浆中天然 Met-enkephalin，并消除应激诱导的血浆中天然和肽酶衍生的 Met-enkephalin 增加。因此，应激诱导的血浆 Met-enkephalin 增加来自于交感神经的释放，而不是肾上腺髓质。然而，交感神经和肾上腺髓质一起似乎并不能完全解释循环中 Met-enkephalin 的基础浓度。肝门静脉血浆中天然 Met-enkephalin 的浓度大于颈动脉中的浓度，提示来自胃肠道的贡献；然而，剖腹术并不能降低血浆中天然 Met-enkephalin 的浓度。在交感神经切断的大鼠中，一些代偿机制导致基础血浆中天然 Met-enkephalin 水平升高。此外，在没有肾上腺髓质的情况下，应激时释放到循环中的 Met-enkephalin 量会代偿性增加。
