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β-肾上腺素能受体和α-肾上腺素能受体在猫睡眠-觉醒周期各阶段调节中的作用。

The role of beta- and alpha-adrenoceptors in the regulation of the stages of the sleep-waking cycle in the cat.

作者信息

Hilakivi I

出版信息

Brain Res. 1983 Oct 24;277(1):109-18. doi: 10.1016/0006-8993(83)90912-5.

Abstract

The effects of beta-adrenergic drugs alone and in combination with alpha-adrenergic drugs on the stages of the sleep-waking cycle were studied in adult cats. Polygraphic sleep recordings of 16 h showed that prenalterol (20 and 40 mg/kg i.p.), a beta 1-adrenoceptor-stimulating drug increased paradoxical sleep (PS) in a dose-related manner during 4-12 h. Salbutamol (40 mg/kg), a beta 2-adrenoceptor-stimulating drug, decreased PS during the first 4 h. Metoprolol (10 and 50 mg/kg), a relatively selective beta 1-adrenoceptor blocking drug, increased drowsy waking during the first 4 h. The larger dose also tended to decrease PS. Already at the lower dose metoprolol partially antagonized the PS increase produced by prazosin, an alpha 1-adrenoceptor blocking drug. Propranolol (5 mg/kg), a beta 1- and beta 2-adrenoceptor blocking drug, which alone decreases PS, antagonized the PS increase induced by phentolamine, an alpha 1- and alpha 2-adrenoceptor blocking drug. Atenolol (5 mg/kg), a poorly lipid-soluble beta-adrenoceptor blocking drug, failed to counteract phentolamine in increasing PS. Metoprolol (10 and 50 mg/kg) and propranolol (5 mg/kg) clearly potentiated the increase in drowsy waking and decrease in deep slow wave sleep and PS induced by clonidine (0.01 mg/kg), an alpha 2-adrenoceptor-stimulating drug. The results support the involvement of beta-adrenoceptors in the regulation of the sleep-waking cycle. A high level of beta-adrenergic activity may facilitate the production of PS. A low level of beta-adrenergic activity, especially in combination with a high level of alpha 2-adrenergic activity, may facilitate the production of drowsy waking. Central alpha 1- and beta 1-adrenoceptors may mediate opposite functions in the regulation of PS.

摘要

在成年猫中研究了β-肾上腺素能药物单独使用以及与α-肾上腺素能药物联合使用对睡眠-觉醒周期各阶段的影响。16小时的多导睡眠记录显示,β1-肾上腺素能受体激动剂普瑞特罗(腹腔注射20和40毫克/千克)在4至12小时内以剂量相关的方式增加了异相睡眠(PS)。β2-肾上腺素能受体激动剂沙丁胺醇(40毫克/千克)在最初4小时内减少了PS。相对选择性的β1-肾上腺素能受体阻断剂美托洛尔(10和50毫克/千克)在最初4小时内增加了困倦觉醒。较大剂量还倾向于减少PS。美托洛尔在较低剂量时就部分拮抗了α1-肾上腺素能受体阻断剂哌唑嗪所产生的PS增加。β1-和β2-肾上腺素能受体阻断剂普萘洛尔(5毫克/千克)单独使用时会减少PS,它拮抗了α1-和α2-肾上腺素能受体阻断剂酚妥拉明所诱导的PS增加。脂溶性较差的β-肾上腺素能受体阻断剂阿替洛尔(5毫克/千克)未能抵消酚妥拉明对PS的增加作用。美托洛尔(10和50毫克/千克)和普萘洛尔(5毫克/千克)明显增强了α2-肾上腺素能受体激动剂可乐定(0.01毫克/千克)所诱导的困倦觉醒增加以及深度慢波睡眠和PS减少。结果支持β-肾上腺素能受体参与睡眠-觉醒周期的调节。高水平的β-肾上腺素能活性可能促进PS的产生。低水平的β-肾上腺素能活性,尤其是与高水平的α2-肾上腺素能活性相结合时,可能促进困倦觉醒的产生。中枢α1-和β1-肾上腺素能受体在PS调节中可能介导相反的功能。

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