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血管加压素诱导清醒大鼠利钠作用:血压、肾前列腺素合成及心房钠尿肽的作用

Vasopressin-induced natriuresis in the conscious rat: role of blood pressure, renal prostaglandin synthesis and the peptide ANF.

作者信息

Lote C J, Thewles A, Wood J A

机构信息

Physiology Department, Medical School, University of Birmingham.

出版信息

J Physiol. 1989 Apr;411:481-91. doi: 10.1113/jphysiol.1989.sp017585.

Abstract
  1. The response to arginine vasopressin (AVP) at doses of 5 and 10 pmol (100 g body weight)-1 h-1 was studied in conscious rats during the infusion of 1% (w/v) dextrose at 11.6 ml h-1 with and without pre-treatment with indomethacin. 2. In the absence of indomethacin AVP infusion induced dose-related increases in sodium output that were positively correlated with increases in mean arterial blood pressure (MAP) and plasma atrial natriuretic factor (ANF) immunoreactivity. Increases in renal prostaglandin E2 (PGE2) synthesis were also associated with AVP infusion. 3. Indomethacin pre-treatment abolished the AVP-induced increases in renal PGE2 synthesis and also the dose-related differences in ANF immunoreactivity. Increases in MAP and sodium output were unaffected at the 10 pmol (100 g body weight)-1 h-1 dose of AVP and only slightly attenuated for the 5 pmol (100 g body weight)-1 h-1 dose. 4. For both series AVP induced marked falls in glomerular filtration rate (GFR) but only small transient falls in effective renal plasma flow. The observed falls in GFR support the view that the natriuresis is due to changes in tubular handling and not in the filtered load of sodium. 5. It is concluded that the natriuresis elicited by AVP is closely related to the pressor action of the hormone but renal PGE2 synthesis and plasma ANF are not responsible for mediating this response.
摘要
  1. 在清醒大鼠中,于输注11.6 ml/h的1%(w/v)葡萄糖期间,研究了剂量为5和10 pmol(100 g体重)-1 h-1的精氨酸加压素(AVP)的反应,同时研究了吲哚美辛预处理和未预处理的情况。2. 在未使用吲哚美辛的情况下,输注AVP会导致钠排出量呈剂量相关增加,这与平均动脉血压(MAP)升高和血浆心钠素(ANF)免疫反应性增加呈正相关。肾前列腺素E2(PGE2)合成增加也与输注AVP有关。3. 吲哚美辛预处理消除了AVP诱导的肾PGE2合成增加以及ANF免疫反应性的剂量相关差异。在10 pmol(100 g体重)-1 h-1剂量的AVP下,MAP和钠排出量的增加未受影响,而在5 pmol(100 g体重)-1 h-1剂量下仅略有减弱。4. 对于两个系列,AVP均导致肾小球滤过率(GFR)显著下降,但有效肾血浆流量仅出现小的短暂下降。观察到的GFR下降支持了利钠是由于肾小管处理变化而非钠滤过负荷变化的观点。5. 得出的结论是,AVP引起的利钠与该激素的升压作用密切相关,但肾PGE2合成和血浆ANF并非介导此反应的原因。

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Cellular mechanism of release of atrial natriuretic factor.心房利钠因子释放的细胞机制。
Biochem Biophys Res Commun. 1984 Oct 30;124(2):443-9. doi: 10.1016/0006-291x(84)91573-0.

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