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杏仁核中的α2肾上腺素能受体控制清醒自发性高血压大鼠的肾交感神经活动和肾功能。

Alpha 2-adrenoceptors in amygdala control renal sympathetic nerve activity and renal function in conscious spontaneously hypertensive rats.

作者信息

Koepke J P, Jones S, DiBona G F

出版信息

Brain Res. 1987 Feb 24;404(1-2):80-8. doi: 10.1016/0006-8993(87)91357-6.

Abstract

The contributions of alpha 2- and beta 2-adrenoceptors in the central amygdaloid nucleus to the increased renal sympathetic nerve activity and decreased urinary sodium excretion resulting from environmental stress (air jet) in conscious spontaneously hypertensive rats (SHR) were examined. Air stress increased mean arterial pressure and renal sympathetic nerve activity (47% from 9.3 +/- 0.8 integrator resets/min), and decreased urinary sodium excretion (38% from 2.4 +/- 0.3 microEq/min/100 g b. wt.). After bilateral administration of guanabenz (2 X 2.5 micrograms) (alpha 2-adrenoceptor agonist) into the central amygdaloid nucleus of the same SHR, air stress had no effect on renal sympathetic nerve activity (+7% from 7.5 +/- 0.8 integrator resets/min) or urinary sodium excretion (+5% from 3.5 +/- 0.4 microEq/min/100 g b. wt.), but still increased mean arterial pressure. These effects of guanabenz were prevented by the prior bilateral administration of the alpha 2-adrenoceptor antagonist, rauwolscine (2 X 15 micrograms), into the central amygdaloid nucleus; rauwolscine alone had no effect on the renal responses to air stress in SHR. Guanabenz in the lateral cerebral ventricle (2 micrograms), the basolateral amygdaloid nucleus (2 X 2.5 micrograms) or a site dorsal to the central amygdaloid nucleus in the area of globus pallidus (2 X 2.5 micrograms) had no effect on the renal sympathetic nerve activity or urinary sodium excretion responses to air stress. Similarly, ICI 118,551 (2 X 1 microgram; beta 2-adrenoceptor antagonist) in the central amygdaloid nucleus had no effect on the renal responses to air stress.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

研究了α2和β2肾上腺素能受体在清醒自发性高血压大鼠(SHR)中央杏仁核中对环境应激(喷气)导致的肾交感神经活动增加和尿钠排泄减少的作用。空气应激增加了平均动脉压和肾交感神经活动(从9.3±0.8积分器重置/分钟增加47%),并减少了尿钠排泄(从2.4±0.3微当量/分钟/100克体重减少38%)。在同一SHR的中央杏仁核双侧注射胍那苄(2×2.5微克)(α2肾上腺素能受体激动剂)后,空气应激对肾交感神经活动(从7.5±0.8积分器重置/分钟增加7%)或尿钠排泄(从3.5±0.4微当量/分钟/100克体重增加5%)没有影响,但仍增加了平均动脉压。预先在中央杏仁核双侧注射α2肾上腺素能受体拮抗剂萝芙辛(2×15微克)可阻止胍那苄的这些作用;单独使用萝芙辛对SHR肾对空气应激的反应没有影响。在侧脑室(2微克)、基底外侧杏仁核(2×2.5微克)或苍白球区域中央杏仁核背侧的一个部位(2×2.5微克)注射胍那苄对肾交感神经活动或尿钠排泄对空气应激的反应没有影响。同样,在中央杏仁核注射ICI 118,551(2×1微克;β2肾上腺素能受体拮抗剂)对肾对空气应激的反应没有影响。(摘要截断于250字)

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