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α-肾上腺素能受体、肾上腺素与原发性高血压中对压力的过度血管收缩反应

Alpha-adrenoceptors, adrenaline, and exaggerated vasoconstrictor response to stress in essential hypertension.

作者信息

Bühler F R, Bolli P, Hulthén U L, Amann F W, Kiowski W

出版信息

Chest. 1983 Feb;83(2 Suppl):304-6. doi: 10.1378/chest.83.2_supplement.304.

Abstract

Stressful sympathetic stimulation by cold pressor test in patients with essential hypertension results in an exaggerated response of the already elevated plasma adrenaline, heart rate, blood pressure, and alpha-adrenoceptor-mediated vasoconstriction when compared with normotensive subjects. The stress-induced increase in adrenaline was correlated with the attendant increase in blood pressure. The stress-induced reduction in forearm flow was reversed during infusion of the postjunctional alpha 1-adrenoceptor blocker prazosin. Therefore, enhanced responses to sympathetic stress, as reflected and perhaps caused by an exaggerated rise in plasma adrenaline, may contribute to an increased alpha 1-adrenoceptor-mediated vasoconstriction in essential hypertension.

摘要

与血压正常的受试者相比,原发性高血压患者通过冷加压试验进行的应激性交感神经刺激会导致血浆肾上腺素、心率、血压以及α-肾上腺素能受体介导的血管收缩反应过度增强,而这些指标原本就已升高。应激诱导的肾上腺素增加与随之而来的血压升高相关。在输注节后α1-肾上腺素能受体阻滞剂哌唑嗪期间,应激诱导的前臂血流量减少得以逆转。因此,对交感神经应激的增强反应,如血浆肾上腺素过度升高所反映的以及可能由此导致的,可能会导致原发性高血压中α1-肾上腺素能受体介导的血管收缩增加。

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