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静脉注射和脑室内注射血管加压素对肾神经活动压力反射控制的影响。

Influence of intravenous and intracerebroventricular vasopressin on baroreflex control of renal nerve traffic.

作者信息

Imaizumi T, Thames M D

出版信息

Circ Res. 1986 Jan;58(1):17-25. doi: 10.1161/01.res.58.1.17.

Abstract

We performed experiments in alpha-chloralose-anesthetized rabbits with vagi sectioned, to determine the influence of intravenous and intracerebroventricular vasopressin on arterial baroreflex control of renal nerve activity. Arterial baroreflex control of renal nerve activity was assessed during phenylephrine-induced increases and nitroglycerin-induced decreases in arterial pressure. Intravenous vasopressin (4 and 40 mU over 1 minute) reduced basal renal nerve activity (from 149 +/- 14 to 101 +/- 13 and 28 +/- 13 impulses/sec) without changing arterial pressure and reduced the sensitivity of the arterial baroreflex control of renal nerve activity. This effect was reversed by vasopressin antagonist (d(CH2)5[Tyr(Me)2]AVP) which blocks vasoconstrictor effects of vasopressin. Intracerebroventricular vasopressin (4, 40, or 400 mU) did not alter basal renal nerve activity or arterial pressure but increased the sensitivity of baroreflex control of renal nerve activity. This effect was not blocked by the vasopressin antagonist. The influence of intravenous vasopressin on basal renal nerve activity was not altered by sinoaortic baroreceptor denervation. In contrast, the inhibitory influence of intravenous vasopressin on lumbar sympathetic nerve activity was abolished by sinoaortic denervation. Finally, intravenous vasopressin inhibited renal nerve activity (by 43 +/- 5%) in six rabbits with spinal cord transection. This effect was abolished by the vasopressin antagonist. We draw the following conclusions from these data: (1) intravenous and intracerebroventricular vasopressin have different effects on basal and baroreflex control of renal nerve activity; (2) these effects are mediated by different vasopressin receptors; (3) the effects of intravenous vasopressin on basal renal nerve activity are not baroreflex dependent, and appear to be mediated by spinal or, possibly, ganglionic mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们在切断迷走神经的α-氯醛糖麻醉兔身上进行实验,以确定静脉注射和脑室内注射血管加压素对肾神经活动的动脉压力感受性反射控制的影响。在去氧肾上腺素引起动脉压升高和硝酸甘油引起动脉压降低期间,评估动脉压力感受性反射对肾神经活动的控制。静脉注射血管加压素(1分钟内注射4和40 mU)可降低基础肾神经活动(从149±14降至101±13和28±13次/秒),而不改变动脉压,并降低动脉压力感受性反射对肾神经活动的控制敏感性。血管加压素拮抗剂(d(CH2)5[Tyr(Me)2]AVP)可逆转此效应,该拮抗剂可阻断血管加压素的血管收缩作用。脑室内注射血管加压素(4、40或400 mU)未改变基础肾神经活动或动脉压,但增加了压力感受性反射对肾神经活动的控制敏感性。此效应未被血管加压素拮抗剂阻断。静脉注射血管加压素对基础肾神经活动的影响不受窦主动脉压力感受器去神经支配的改变。相反,静脉注射血管加压素对腰交感神经活动的抑制作用被窦主动脉去神经支配所消除。最后,静脉注射血管加压素抑制了6只脊髓横断兔的肾神经活动(降低43±5%)。此效应被血管加压素拮抗剂消除。我们从这些数据得出以下结论:(1)静脉注射和脑室内注射血管加压素对肾神经活动的基础和压力感受性反射控制有不同影响;(2)这些效应由不同血管加压素受体介导;(3)静脉注射血管加压素对基础肾神经活动的影响不依赖于压力感受性反射,似乎由脊髓或可能由神经节机制介导。(摘要截短于250字)

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