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大鼠外周β-肾上腺素能受体与应激诱导的高胆固醇血症

Peripheral beta-adrenoreceptors and stress-induced hypercholesterolemia in rats.

作者信息

Brennan F X, Cobb C L, Silbert L H, Watkins L R, Maier S F

机构信息

Psychology Department, University of Colorado, Boulder 80309, USA.

出版信息

Physiol Behav. 1996 Nov;60(5):1307-10. doi: 10.1016/s0031-9384(96)00255-7.

Abstract

Three experiments were conducted examining the contribution of beta-adrenergic receptors to stress-induced cholesterol increases. Rats were exposed to 3 90-min sessions of inescapable tailshock, or left undisturbed in their home cage. Propranolol, a nonselective beta-blocker, attenuated the stress-induced cholesterol increase when administered prior to the daily shock session. Atenolol, a beta-1 specific antagonist, also attenuated the stress-induced cholesterol increase. Butoxamine, a beta-2 specific antagonist, had no effect on the stress-induced cholesterol increases. Results are discussed in terms of catecholamine-stimulated free fatty acid (FFA) release as a potential mechanism for producing stress-induced hypercholesterolemia.

摘要

进行了三项实验,研究β-肾上腺素能受体在应激诱导的胆固醇升高过程中的作用。将大鼠暴露于3次每次90分钟的不可逃避的尾部电击下,或者让它们在其饲养笼中不受干扰。普萘洛尔,一种非选择性β阻滞剂,在每日电击前给药时可减弱应激诱导的胆固醇升高。阿替洛尔,一种β-1特异性拮抗剂,也可减弱应激诱导的胆固醇升高。丁氧胺,一种β-2特异性拮抗剂,对应激诱导的胆固醇升高没有影响。结果从儿茶酚胺刺激的游离脂肪酸(FFA)释放的角度进行了讨论,认为这是产生应激诱导的高胆固醇血症的一种潜在机制。

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