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首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Relative atrial natriuretic peptide deficiency and inadequate renin and angiotensin II suppression in obese hypertensive men
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Relative atrial natriuretic peptide deficiency and inadequate renin and angiotensin II suppression in obese hypertensive men

机译：肥胖高血压男性相对性心房利钠肽缺乏症和肾素和血管紧张素II抑制不足

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Obesity is a strong risk factor for hypertension, but the mechanisms by which obesity leads to hypertension are incompletely understood. On this background, we assessed dietary sodium intake, serum levels of natriuretic peptides (NPs), and the activity of the renin-angiotensin system in 63 obese hypertensive men (obeseHT: body mass index, ≥30.0 kg/m; 24-hour ambulatory blood pressure, ≥130/80 mm Hg), in 40 obese normotensive men (obeseNT: body mass index, ≥30.0 kg/m; 24-hour ambulatory blood pressure, <130/80 mm Hg), and in 27 lean normotensive men (leanNT: body mass index, 20.0-24.9 kg/m; 24-hour ambulatory blood pressure, <130/80 mm Hg). All study subjects were medication free. As a surrogate estimate for dietary sodium intake, we measured sodium excretion in a 24-hour urine collection and we measured serum levels of midregional proatrial NP and plasma levels of renin and angiotensin II. The obese men had higher mean (±SD) urinary sodium excretion (obeseHT, 213.6±85.2 mmol; obeseNT, 233.0±70.0 mmol) than the lean normotensive men (leanNT, 155.5±51.7 mmol; P=0.003). ObeseHT had lower (median [interquartile range]) serum midregional proatrial NP levels (49.2 [37.3-64.7] pmol/L) than leanNT (69.3 [54.3-82.9] pmol/L; P=0.003), whereas obeseNT had midregional proatrial NP levels in between (54.1 [43.2-64.7] pmol/L); obeseNT had lower (median [interquartile range]) plasma levels of renin (5.0 [3.0-8.0] mIU/L versus 9.0 [4.0-18.0]) and angiotensin II (2.4 [1.5-3.5] pmol/L versus 4.2 [2.2-7.9]) than obeseHT (P≤0.049), whereas obeseHT had similar plasma levels of renin and angiotensin II as leanNT (P≥0.19). Thus, despite a high sodium intake and a high blood pressure, obese hypertensive men have a relative NP deficiency and an inadequate renin-angiotensin system suppression.
机译：肥胖是高血压的重要危险因素，但肥胖导致高血压的机制尚不完全清楚。在此背景下，我们评估了63名肥胖高血压男性的饮食钠摄入量，利钠肽（NP）的血清水平以及肾素-血管紧张素系统的活性（肥胖：体重指数，≥30.0 kg / m; 24小时门诊血压，≥130/80 mm Hg），40名肥胖的血压正常男人（肥胖：体重指数，≥30.0 kg / m; 24小时动态血压，<130/80 mm Hg）和27名瘦血压正常的男人（leanNT：体重指数，20.0-24.9 kg / m; 24小时动态血压，<130/80 mm Hg）。所有研究对象均无药物治疗。作为膳食钠摄入量的替代估算，我们测量了24小时尿液收集中的钠排泄量，并测量了中部区域心房NP的血清水平以及肾素和血管紧张素II的血浆水平。肥胖男性比正常血压男性（leanNT，155.5±51.7 mmol; P = 0.003）有更高的平均尿尿钠排泄（obseHT，213.6±85.2 mmol; obeseNT，233.0±70.0 mmol）。 ObeseHT的血清中区原发性NP水平（中位数[四分位数范围]）较低（49.2 [37.3-64.7] pmol / L），低于leanNT（69.3 [54.3-82.9] pmol / L; P = 0.003），而obeseNT的中部原发性NP水平较低介于（54.1 [43.2-64.7] pmol / L）之间的水平; obeseNT的血浆中肾素（5.0 [3.0-8.0] mIU / L与9.0 [4.0-18.0]）和血管紧张素II（2.4 [1.5-3.5] pmol / L与4.2 [2.2-2.2] [7.9]]高于肥胖者（P≤0.049），而肥胖者血浆中的肾素和血管紧张素II水平与leanNT（P≥0.19）相似。因此，尽管钠摄入量高和血压高，肥胖的高血压男性仍具有相对的NP缺乏和肾素-血管紧张素系统抑制不足。

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