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[不同病因的动脉高血压患者肾血管床中的前列腺素]

[Prostaglandins in the renal vascular bed in arterial hypertension of different etiologies].

作者信息

Nekrasova A A, Klembovskiĭ A A, Uchitel' I A, Matveeva L S, Shpil'kin V M

出版信息

Kardiologiia. 1983 Apr;23(4):16-21.

PMID:6345886
Abstract

Levels of PGE2, PGF2 alpha and renin activity were measured in renal venous blood of 29 patients with essential hypertension (EH), 23 patients with renovascular hypertension (RVH) and 10 patients with unilateral pyelonephritis and high arterial hypertension. The pattern of change in renal venous PG content was found to be related to the type of renal lesion: the level of PGE2 was lowered and PGF2 alpha/PGF2 ratio increased in the blood outflow from the kidneys of EH patients and from ischemized kidneys of RVH patients as compared to similar parameters in the outflow from contralateral kidneys of patients with RVH and pyelonephritis. Venous levels of both PGs were the highest in pyelonephritis-affected kidneys. Renal venous PG levels go down in all cases as the disease grows older. An acute drop in arterial pressure is accompanied with increased withdrawal of PGF2 alpha from the kidneys and enhanced renin activity in renal veins, while PGE2 drops simultaneously. PGF2 and PGE2 showing different trends of change in response to falling arterial pressure suggests increased transition of PGE2 to PGF2 alpha under the effect of enhanced PG-9-ketodehydrogenase activity. In the abdominal aorta, the scope of drop in arterial pressure correlates to the change in PGF2 alpha level, that is an evidence of PG direct involvement in the autoregulation of renal blood flow.

摘要

对29例原发性高血压(EH)患者、23例肾血管性高血压(RVH)患者以及10例单侧肾盂肾炎合并重度高血压患者的肾静脉血中前列腺素E2(PGE2)、前列腺素F2α(PGF2α)水平及肾素活性进行了测定。结果发现,肾静脉前列腺素含量的变化模式与肾脏病变类型有关:与RVH和肾盂肾炎患者对侧肾脏流出的血液中的类似参数相比,EH患者以及RVH患者缺血肾脏流出的血液中PGE2水平降低,PGF2α/PGF2比值升高。在受肾盂肾炎影响的肾脏中,两种前列腺素的静脉水平最高。随着疾病进展,所有病例的肾静脉前列腺素水平均下降。动脉压急性下降时,肾脏对PGF2α的摄取增加,肾静脉肾素活性增强,而PGE2同时下降。PGF2和PGE2在动脉压下降时呈现不同的变化趋势,提示在PG-9-酮脱氢酶活性增强的作用下,PGE2向PGF2α的转化增加。在腹主动脉中,动脉压下降的幅度与PGF2α水平的变化相关,这证明前列腺素直接参与肾血流的自身调节。

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1
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Kardiologiia. 1983 Apr;23(4):16-21.
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