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心房利钠肽可对抗血管紧张素 II 诱导的肾功能损害。

Atrial natriuretic peptide counteracts angiotensin-II-induced impairment of renal function.

作者信息

Schafferhans K, Heidbreder E, Hummel S, Heidland A

机构信息

Department of Medicine, University of Würzburg, F.R.G.

出版信息

Z Kardiol. 1988;77 Suppl 2:78-84.

PMID:2970179
Abstract

The present study was designed to investigate the effect of atrial natriuretic peptide (ANP) on angiotensin II (AT II)-induced impairment of renal function. Female Sprague Dawley were used in this study. After anesthesia and surgical procedure, animals were infused with AT II at two different doses (group I, 15 micrograms/kg BW/min and group II, 15 ng/kg BW/min) into the left renal artery. Subsequently, alpha-ANP was infused intrarenally (left kidney, LK) at 2 micrograms/kg BW/min. Controls received isotonic saline only. In all cases the right and noninfused kidney (RK) served as control organ. In all animals, AT II led to a dose-dependent compromise of kidney function of the LK. Glomerular filtration rate (GFR) had decreased to 0.16 +/- 0.06 ml/min and 0.41 +/- 0.12 ml/min in group I and II, respectively. Subsequent ANP infusion induced a significant increase of GFR to 0.83 +/- 0.23 (p less than 0.01) and 0.99 +/- 0.20 (p less than 0.05) ml/min in group I and II, respectively. Urinary volume (V) exhibited a slight but not significant increase following AT II infusion. ANP infusion led to a highly significant increase of V in both groups. A less pronounced, but significant increase of absolute sodium excretion of the LK was observed in both groups after AT II infusion. Absolute potassium excretion did not change in this phase of the experiment. ANP infusion induced a significant increase in both parameters. Isotonic saline had no effect on all parameters measured. Mean arterial pressure (MAP) had increased dose dependent following AT II infusion. After ANP infusion, a significant diminution of MAP to basal values was obtained from both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究旨在探讨心房利钠肽(ANP)对血管紧张素II(AT II)所致肾功能损害的影响。本研究使用雌性斯普拉格-道利大鼠。麻醉及手术后,将动物分为两组,分别以两种不同剂量(I组,15微克/千克体重/分钟;II组,15纳克/千克体重/分钟)向左肾动脉输注AT II。随后,以2微克/千克体重/分钟的剂量向左肾(LK)肾内输注α-ANP。对照组仅接受等渗盐水。在所有情况下,右肾及未输注的肾(RK)作为对照器官。在所有动物中,AT II导致LK肾功能呈剂量依赖性损害。I组和II组的肾小球滤过率(GFR)分别降至0.16±0.06毫升/分钟和0.41±0.12毫升/分钟。随后输注ANP后,I组和II组的GFR分别显著增加至0.83±0.23(p<0.01)和0.99±0.20(p<0.05)毫升/分钟。输注AT II后尿量(V)略有增加但不显著。输注ANP导致两组尿量均显著增加。输注AT II后,两组LK的绝对钠排泄量均有不太明显但显著的增加。在实验的这一阶段,绝对钾排泄量未发生变化。输注ANP导致这两个参数均显著增加。等渗盐水对所有测量参数均无影响。输注AT II后平均动脉压(MAP)呈剂量依赖性升高。输注ANP后,两组的MAP均显著降至基础值。(摘要截断于250字)

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