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前列腺素和血管紧张素II在心房钠尿肽诱导的利钠作用中的作用。

Role of prostaglandin and angiotensin II in ANP-induced natriuresis.

作者信息

Salazar F J, Bolterman R, Hernandez I, Quesada T, Romero J C

机构信息

Department of Physiology and Biophysics, Mayo Medical School, Rochester, MN 55905.

出版信息

Agents Actions Suppl. 1987;22:111-23. doi: 10.1007/978-3-0348-9299-5_12.

DOI:10.1007/978-3-0348-9299-5_12
PMID:2963506
Abstract

The aim of the present study was to examine if the natriuresis induced by a dose of ANP that does not alter glomerular filtration rate (GFR) or mean arterial pressure (MAP) is accompanied by changes in renin release urinary excretion of prostaglandins and intrarenal blood flow distribution. It was found that the intrarenal infusion of ANP (8-33) at a dose of 0.05 micrograms/kg min in seven anaesthetized dogs did not produce any change in GFR or MAP, but its natriuretic effect was similar to that induced by a larger dose (0.3 micrograms/kg min, n = 5) that produces significant changes in both MAP and GFR. The natriuresis induced by the lower dose of ANP was associated with a redistribution of RBF to the deep cortical nephrons and with an increase (p less than 0.05) in urinary excretion of prostaglandins E2 and 6 keto-F1 alpha. Renin secretion rate decreased by a 54% (p less than 0.05). The role of angiotensin II (AII) suppression on the natriuresis induced by ANP was examine in another experimental group (n = 6). It was found that the infusion of ANP during fixed intrarenal levels of AII produced a natriuretic effect that was significantly lower (38%) than that produced by the infusion of ANP alone. The results of this study show that the natriuresis induced by ANP is not necessarily produced by an increase in GFR and is associated with a redistribution of RBF to the deep cortex an increase in urinary excretion of prostaglandins and a decrease of renin release. These results also suggest that the natriuretic effect of ANP is partly mediated by the intrarenal suppression of AII.

摘要

本研究的目的是检验在不改变肾小球滤过率(GFR)或平均动脉压(MAP)的情况下,一定剂量的心房利钠肽(ANP)所诱导的利钠作用是否伴随着肾素释放、前列腺素尿排泄及肾内血流分布的变化。研究发现,在7只麻醉犬中,以0.05微克/千克·分钟的剂量肾内输注ANP(8 - 33),GFR或MAP未发生任何变化,但其利钠作用与较大剂量(0.3微克/千克·分钟,n = 5)所诱导的相似,而较大剂量会使MAP和GFR均发生显著变化。较低剂量ANP所诱导的利钠作用与肾血流(RBF)重新分布至深层皮质肾单位以及前列腺素E2和6 - 酮 - F1α的尿排泄增加(p < 0.05)相关。肾素分泌率下降了54%(p < 0.05)。在另一实验组(n = 6)中,研究了血管紧张素II(AII)抑制对ANP诱导的利钠作用的影响。结果发现,在肾内AII水平固定时输注ANP所产生的利钠作用明显低于单独输注ANP所产生的利钠作用(低38%)。本研究结果表明,ANP诱导的利钠作用不一定由GFR增加所致,而是与RBF重新分布至深层皮质、前列腺素尿排泄增加以及肾素释放减少有关。这些结果还表明,ANP的利钠作用部分是由肾内AII抑制介导的。

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