[The possible mechanism of the noradrenaline enhancement of the arterial baroreceptor reflex].

V S Eremeev, V A Smirnov, R S Khrustaleva, V A Tsyrlin, Iu I Shcherbin
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引用次数: 0

Abstract

In anaesthetized cats intravenous infusion of norepinephrine induced the increase in arterial pressure and suppression of renal nerve electrical activity. The latter followed the infusion was stopped and arterial pressure returned toward control. The baroreflex suppression of sympathetic activity associated with norepinephrine increased in the case of preliminary mechanical damage to blood-brain barrier. Duration and intensity of the sympathetic activity suppression following norepinephrine infusion depended on the magnitude of hypertensive reaction and the rate of elevating in arterial pressure under the action of norepinephrine. Norepinephrine at the similar concentrations did not depress sympathetic activity if the arterial pressure was stabilized on the resting level. These data support the supposition that the elevation of arterial pressure due to norepinephrine infusion increases the ability of catecholamine to enter brain and in this way activates the central limb of arterial baroreceptor reflex.

去甲肾上腺素增强动脉压力感受器反射的可能机制。
在麻醉猫中静脉输注去甲肾上腺素引起动脉压升高和肾神经电活动抑制。后一种情况是停止注射,动脉压恢复正常。在血脑屏障初步机械损伤的情况下,与去甲肾上腺素相关的交感神经活动的压反射抑制增加。去甲肾上腺素输注后交感神经活动抑制的持续时间和强度取决于高血压反应的程度和在去甲肾上腺素作用下动脉压升高的速率。如果动脉压稳定在静息水平,相同浓度的去甲肾上腺素不会抑制交感神经活动。这些数据支持了一种假设,即由于去甲肾上腺素输注引起的动脉压力升高增加了儿茶酚胺进入大脑的能力,从而激活了动脉压力感受器反射的中央肢体。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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