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高血压男性容量负荷增加时肾素抑制与心房利钠肽(α-心钠素)之间的显著关系。

Significant relationship between renin suppression and atrial natriuretic peptide (alpha-hANP) during volume loading in hypertensive men.

作者信息

Andersson O K, Persson B, Wysocki M, Berglund G, Towle A C, Aurell M, Hedner J, Hedner T

出版信息

Acta Med Scand. 1987;221(2):137-42. doi: 10.1111/j.0954-6820.1987.tb01257.x.

Abstract

We have studied eight men with moderate hypertension to determine the atrial natriuretic peptide (alpha-hANP) response to acute volume expansion. Rapid infusion of 1,000 ml 0.9% saline (10-20 min) caused an increase in central venous pressure (4.7 +/- 1.6 cmH2O) while blood pressure and pulse pressure (arterial baroreceptor load) did not change. Stroke volume and heart rate were not affected by the volume load but plasma renin activity (PRA) was significantly suppressed (from 0.83 +/- 0.14 to 0.68 +/- 0.34 microgram AI I/ml-h; p less than 0.01). A significant hemodilution was also observed. Renal sodium excretion was significantly increased. Arterial alpha-hANP increased significantly from 21.1 +/- 6.1 to 30.5 +/- 4.0 pmol/l (p less than 0.02) during volume expansion. There was a significant correlation between corrected plasma volume increase (urine volume subtracted from the infused volume) and alpha-hANP plasma elevation (r = 0.78; p less than 0.05). There was also a significant negative correlation between changes alpha-hANP and PRA (r = -0.78, p less than 0.05). We conclude that only moderate volume loading in human hypertensives is a mechanism for increase in plasma alpha-hANP levels. The significant negative correlation between changes in alpha-hANP and PRA suggests that alpha-hANP may be the humoral factor at least partly responsible for suppression of renin in hypertensive man. Since increased fluid volume also affects sympathetic renal efferents as well as vasopressin secretion, our observed relationship between volume load and renin may well be related also to such mechanisms.

摘要

我们研究了8名中度高血压男性,以确定心房利钠肽(α-hANP)对急性容量扩张的反应。快速输注1000毫升0.9%生理盐水(10 - 20分钟)导致中心静脉压升高(4.7±1.6厘米水柱),而血压和脉压(动脉压力感受器负荷)未改变。每搏输出量和心率不受容量负荷影响,但血浆肾素活性(PRA)显著受到抑制(从0.83±0.14降至0.68±0.34微克血管紧张素I/毫升·小时;p<0.01)。还观察到明显的血液稀释。肾钠排泄显著增加。容量扩张期间,动脉α-hANP从21.1±6.1显著增加至30.5±4.0皮摩尔/升(p<0.02)。校正后的血浆容量增加(输注量减去尿量)与α-hANP血浆升高之间存在显著相关性(r = 0.78;p<0.05)。α-hANP变化与PRA之间也存在显著负相关(r = -0.78,p<0.05)。我们得出结论,在人类高血压患者中,仅适度的容量负荷是血浆α-hANP水平升高的一种机制。α-hANP变化与PRA之间的显著负相关表明,α-hANP可能是至少部分负责抑制高血压患者肾素的体液因子。由于增加的液体容量也会影响肾交感传出神经以及抗利尿激素分泌,我们观察到的容量负荷与肾素之间的关系很可能也与这些机制有关。

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