Gallen I W, Rosa R M, Esparaz D Y, Young J B, Robertson G L, Batlle D, Epstein F H, Landsberg L
Department of Medicine, Northwestern University Medical School, Chicago, IL, USA.
Am J Kidney Dis. 1998 Jan;31(1):19-27. doi: 10.1053/ajkd.1998.v31.pm9428447.
Dietary potassium restriction increases sodium and chloride retention, whereas potassium administration promotes both diuresis and natriuresis. In epidemiologic and clinical studies, potassium intake is inversely related to blood pressure and is lower in blacks than in whites. The present studies examined the mechanism by which potassium restriction fosters sodium conservation and the impact of race on this response. Twenty-one healthy black and white men and women ingested an isocaloric, potassium-restricted diet (20 mmol/d) containing 180 mmol/d of sodium with and without a potassium supplement (80 mmol/d) for 9 days on two occasions. Additionally, eight of these subjects ingested the same diets for 3 days followed by a water load to determine free water clearance before and during the early phase of dietary potassium restriction. During potassium restriction, mean arterial pressure (MAP) derived from 24-hour blood pressure measurements was higher (85.7 +/- 1.6 mm Hg v 82.0 +/- 1.3 mm Hg; P < 0.001), cumulative sodium excretion lower (984 +/- 59 mmol/d v 1,256 +/- 58 mmol/d; P < 0.001), and weight greater (71.1 +/- 2.1 kg v 69.3 +/- 2.2 kg; P < 0.001). Blacks displayed no greater increase in MAP, although they excreted less sodium overall and less potassium on the potassium-supplemented diet. After a water load, minimum urine osmolality (Uosm) was lower (53.0 +/- 3.0 mOsm/L v 65.6 +/- 3.5 mOsm/L; P = 0.01) and free water clearance greater (4.44 +/- 0.59 mL/min v3.72 +/- 0.58 mL/min; P = 0.009) during potassium restriction. In conclusion, in healthy, normotensive subjects, potassium restriction was associated with an increase in blood pressure and volume expansion effected by increased renal sodium and chloride retention. Potassium restriction was also associated with increased free water clearance and enhanced diluting capacity consistent with augmentation of Na+, K+:2Cl- cotransporter activity in the thick ascending limb of Henle. This mechanism may play an important role in the renal adaptation required for potassium conservation, but at the expense of sodium chloride retention and an elevation in blood pressure.
限制饮食中钾的摄入会增加钠和氯的潴留，而补充钾则会促进利尿和排钠。在流行病学和临床研究中，钾的摄入量与血压呈负相关，且黑人的钾摄入量低于白人。本研究探讨了限制钾摄入促进钠潴留的机制以及种族对这种反应的影响。21名健康的黑人和白人男性及女性分两次连续9天摄入等热量、低钾饮食（20 mmol/d），该饮食含钠180 mmol/d，其中一次同时补充钾（80 mmol/d），另一次不补充。此外，其中8名受试者先按相同饮食摄入3天，然后进行水负荷试验，以测定在饮食钾限制早期及之前的自由水清除率。在钾限制期间，通过24小时血压测量得出的平均动脉压（MAP）较高（85.7±1.6 mmHg对82.0±1.3 mmHg；P<0.001），累积钠排泄量较低（984±59 mmol/d对1256±58 mmol/d；P<0.001），体重增加（71.1±2.1 kg对69.3±2.2 kg；P<0.001）。黑人的MAP升高幅度并不更大，尽管他们总体上钠排泄较少，且在补充钾的饮食中钾排泄也较少。水负荷后，在钾限制期间最低尿渗透压（Uosm）较低（53.0±3.0 mOsm/L对65.6±3.5 mOsm/L；P = 0.01），自由水清除率较高（4.44±0.59 mL/min对3.72±0.58 mL/min；P = 0.009）。总之，在健康的血压正常受试者中，限制钾摄入与血压升高及因肾钠和氯潴留增加导致的容量扩张有关。钾限制还与自由水清除率增加和稀释能力增强有关，这与髓袢升支粗段中Na⁺、K⁺:2Cl⁻共转运体活性增强一致。这种机制可能在钾潴留所需的肾脏适应性变化中起重要作用，但代价是氯化钠潴留和血压升高。
