人α-心房利钠肽生理增量的急性效应。

Acute effects of physiological increments of alpha-atrial natriuretic peptide in man.

作者信息

Brown J, O'Flynn M A

机构信息

Physiological Laboratory, University of Cambridge, United Kingdom.

出版信息

Kidney Int. 1989 Oct;36(4):645-52. doi: 10.1038/ki.1989.241.

DOI:10.1038/ki.1989.241

PMID:2530384

Abstract

Seven dehydrated volunteers received three hour infusions of 0.8 pmol kg-1 min-1 of human alpha-atrial natriuretic peptide (h-alpha ANP) or vehicle alone (Ve) in a single-blind, randomized cross-over design. H-alpha ANP infusion increased plasma h-alpha ANP from 4.2 +/- 0.4 to 20.3 +/- 6.4 pm. H-alpha ANP suppressed plasma renin activity from 3.30 +/- 0.48 to 1.37 +/- 0.35 ng ml-1 hr-1 (P less than 0.001 vs. Ve). Plasma aldosterone was unaltered by h-alpha ANP. Fractional excretion of filtered sodium (FENa) changed from 0.92 +/- 0.09 to 1.13 +/- 0.16% with h-alpha ANP, and from 1.02 +/- 0.09 to 0.69 +/- 0.11% with Ve (P less than 0.01 h-alpha ANP vs. Ve). FEK was unchanged. FEpo4 increased from 7.2 +/- 1.2 to 9.2 +/- 1.2% and FELi from 22.1 +/- 1.4 to 24.9 +/- 3.0% with h-alpha ANP (both P less than 0.05 vs. Ve). H-alpha ANP decreased mean urinary osmolality by approximately 150 mOsmol kg-1 compared to Ve (P less than 0.01). GFR, RPF and filtration fraction were unchanged by h-alpha ANP, H-alpha ANP was associated with a significant tachycardia (P less than 0.01 vs. Ve) but with no significant change in arterial pressure. These results suggest that small increments of plasma h-alpha ANP, mimicking physiological changes, are natriuretic at least partly by reducing proximal tubular reabsorption of sodium, and also impair urinary concentration.

摘要

七名脱水志愿者采用单盲、随机交叉设计，接受了每千克体重每分钟0.8皮摩尔人α - 心房利钠肽（h-α ANP）或仅接受载体（Ve）的三小时输注。h-α ANP输注使血浆h-α ANP从4.2±0.4升高至20.3±6.4皮摩尔。h-α ANP将血浆肾素活性从3.30±0.48抑制至1.37±0.35纳克每毫升每小时（与Ve相比，P<0.001）。h-α ANP未改变血浆醛固酮。h-α ANP作用下，滤过钠分数排泄（FENa）从0.92±0.09变为1.13±0.16%，而Ve作用下从1.02±0.09变为0.69±0.11%（h-α ANP与Ve相比，P<0.01）。FEK未改变。h-α ANP作用下，FEpo4从7.2±1.2升高至9.2±1.2%，FELi从22.1±1.4升高至24.9±3.0%（两者与Ve相比，P均<0.05）。与Ve相比，h-α ANP使平均尿渗透压降低约150毫摩尔每千克（P<0.01）。h-α ANP未改变肾小球滤过率、肾血浆流量和滤过分数。h-α ANP与显著的心动过速相关（与Ve相比，P<0.01），但动脉压无显著变化。这些结果表明，模仿生理变化的血浆h-α ANP小幅度升高至少部分通过减少近端肾小管对钠的重吸收而具有利钠作用，并且还损害尿液浓缩功能。