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血管加压素促进通过迷走神经传入介导的肾神经活动抑制。

Vasopressin facilitates inhibition of renal nerve activity mediated through vagal afferents.

作者信息

Gupta B N, Abboud A L, Floras J S, Aylward P E, Abboud F M

出版信息

Am J Physiol. 1987 Jul;253(1 Pt 2):H1-7. doi: 10.1152/ajpheart.1987.253.1.H1.

Abstract

We measured the effect of vasopressin (8 mU X kg-1 X min-1) on reflex inhibition of renal sympathetic nerve activity induced by volume expansion in 13 sinoaortic-denervated anesthetized rabbits. Volume expansion increased left ventricular end-diastolic pressure (LVEDP) from 5.1 +/- 0.7 to 14.1 +/- 1.4 mmHg and decreased renal nerve activity (RNA) from 57.4 +/- 6.9 to 30.2 +/- 5.6 impulses/s. Infusion of vasopressin elevated LVEDP from 6.0 +/- 1.0 to 7.3 +/- 1.1 mmHg and decreased RNA from 61.8 +/- 7.2 to 47.1 +/- 6.3 impulses/s. Heart rate fell from 243 +/- 7 to 231 +/- 9 beats/min; no other significant hemodynamic changes were seen. During the infusion of vasopressin, volume expansion increased LVEDP to 13.7 +/- 1.2 mmHg and decreased RNA to 17.0 +/- 4.2 impulses/s. The slopes relating the percent decrease in RNA to the rise in LVEDP were calculated from values of RNA recorded at several levels of LVEDP. The slope averaged -6.2 +/- 1.1%/mmHg before vasopressin and nearly doubled (-11.9 +/- 1.8%/mmHg) during vasopressin. Infusion of placebo (saline) instead of vasopressin did not alter the reflex inhibition of nerve activity. Bilateral vagotomy abolished the decrease in resting nerve activity that occurred during infusion of vasopressin as well as the reflex inhibition of RNA. These data demonstrate that vasopressin facilitates the reflex inhibition of renal sympathetic nerve activity associated with increases in LVEDP and mediated through vagal afferents.

摘要

我们在13只经窦主动脉去神经支配的麻醉兔中,测量了血管加压素(8 mU·kg⁻¹·min⁻¹)对容量扩张诱导的肾交感神经活动反射性抑制的影响。容量扩张使左心室舒张末期压力(LVEDP)从5.1±0.7 mmHg升高至14.1±1.4 mmHg,并使肾神经活动(RNA)从57.4±6.9次/秒降至30.2±5.6次/秒。输注血管加压素使LVEDP从6.0±1.0 mmHg升高至7.3±1.1 mmHg,并使RNA从61.8±7.2次/秒降至47.1±6.3次/秒。心率从243±7次/分钟降至231±9次/分钟;未见其他显著的血流动力学变化。在输注血管加压素期间,容量扩张使LVEDP升高至13.7±1.2 mmHg,并使RNA降至17.0±4.2次/秒。根据在几个LVEDP水平记录的RNA值计算RNA降低百分比与LVEDP升高之间的斜率。血管加压素前斜率平均为-6.2±1.1%/mmHg,血管加压素期间几乎翻倍(-11.9±1.8%/mmHg)。输注安慰剂(生理盐水)而非血管加压素未改变神经活动的反射性抑制。双侧迷走神经切断术消除了输注血管加压素期间发生的静息神经活动降低以及RNA的反射性抑制。这些数据表明,血管加压素促进了与LVEDP升高相关且通过迷走传入神经介导的肾交感神经活动的反射性抑制。

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