Kjolby M J, Kompanowska-Jezierska E, Wamberg S, Bie P
Department of Physiology and Pharmacology, Institute of Medical Biology, University of Southern Denmark, Odense, Denmark.
Acta Physiol Scand. 2005 Jul;184(3):225-34. doi: 10.1111/j.1365-201X.2005.01452.x.
The operating range of the renin-angiotensin-aldosterone system is ill-defined. This study quantifies renin-angiotensin-aldosterone system activity as a function of sodium intake.
Renin-angiotensin-aldosterone system variables were measured daily after a sudden reduction in sodium intake (3.0-0.5 mmol kg(-1) day(-1)) or at steady states generated by eight levels of sodium intake (0.5-8.0 mmol kg(-1) day(-1)). Potassium intake was 2.79 +/- 0.03 mmol kg(-1) day(-1). Arterial blood pressure was measured invasively. Hormone concentrations were determined by radioimmunoassays. Glomerular filtration rate and plasma volume were determined by standard methods.
Sudden sodium intake reduction doubled plasma renin activity and angiotensin II, and tripled aldosterone on day 1 with only small non-significant additional changes on the following days. Different levels of sodium intake did not affect arterial blood pressure, heart rate, and plasma concentrations of sodium, angiotensinogen, atrial natriuretic peptide, vasopressin, glomerular filtration rate and diuresis. With increasing sodium intake, plasma volume increased by 0.47 +/- 0.04 mL (kg body mass)(-1) (unit increase in Na intake)(-1) (P < 0.01), and plasma potassium decreased with the slope -0.038 mm (mmol Na+ intake) (kg body mass)(-1) day(-1) (P = 0.001) while plasma renin-activity, angiotensin II, and aldosterone decreased systematically as expected.
A step reduction in sodium intake alters renin-angiotensin-aldosterone system activity on day 1 with little further change the subsequent 4 days. Week-long increases in sodium intake decreases renin-angiotensin-aldosterone system activity, increases plasma volume, and decreases plasma potassium. Isolated decreases in sodium intake increase aldosterone secretion via volume-mediated action on the renin-angiotensin system and via increases in plasma potassium.
肾素 - 血管紧张素 - 醛固酮系统的作用范围尚不明确。本研究将肾素 - 血管紧张素 - 醛固酮系统活性定量为钠摄入量的函数。
在钠摄入量突然减少(从3.0 mmol·kg⁻¹·天⁻¹降至0.5 mmol·kg⁻¹·天⁻¹)后,或在由八个钠摄入水平(0.5 - 8.0 mmol·kg⁻¹·天⁻¹)产生的稳定状态下,每日测量肾素 - 血管紧张素 - 醛固酮系统变量。钾摄入量为2.79±0.03 mmol·kg⁻¹·天⁻¹。采用有创测量动脉血压。通过放射免疫分析法测定激素浓度。采用标准方法测定肾小球滤过率和血浆容量。
钠摄入量突然减少使血浆肾素活性和血管紧张素II在第1天增加一倍,醛固酮增加两倍,在随后几天仅有微小的、无统计学意义的额外变化。不同水平的钠摄入量不影响动脉血压、心率以及血浆钠、血管紧张素原、心房利钠肽、血管加压素、肾小球滤过率和尿量的浓度。随着钠摄入量增加,血浆容量以0.47±0.04 mL·(kg体重)⁻¹·(单位钠摄入量增加)⁻¹的幅度增加(P < 0.01),血浆钾以斜率-0.038 mmol·[(mmol钠摄入量)·(kg体重)⁻¹·天⁻¹]⁻¹下降(P = 0.001),而血浆肾素活性、血管紧张素II和醛固酮如预期的那样系统性下降。
钠摄入量的逐步减少在第1天改变肾素 - 血管紧张素 - 醛固酮系统活性,在随后4天几乎没有进一步变化。为期一周的钠摄入量增加会降低肾素 - 血管紧张素 - 醛固酮系统活性,增加血浆容量,并降低血浆钾水平。单纯的钠摄入量减少通过对肾素 - 血管紧张素系统的容量介导作用以及血浆钾的增加来增加醛固酮分泌。