Morris R C, Sebastian A, Forman A, Tanaka M, Schmidlin O
Department of Medicine, General Clinical Research Center, University of California, San Francisco 94143-0126, USA.
Hypertension. 1999 Jan;33(1):18-23. doi: 10.1161/01.hyp.33.1.18.
-Normotensive salt sensitivity, a putative precursor of hypertension, might be quite frequent in African Americans (blacks) and less frequent in Caucasian Americans (whites), but only when dietary potassium is deficient and not when maintained well within the normal range. We tested this hypothesis in 41 metabolically controlled studies of 38 healthy normotensive men (24 blacks, 14 whites) who ate a basal diet low in sodium (15 mmol/d) and marginally deficient in potassium (30 mmol/d) for 6 weeks. Throughout the last 4 weeks, NaCl was loaded (250 mmol/d); throughout the last 3, potassium was supplemented (as potassium bicarbonate) to either mid- or high-normal levels, 70 and 120 mmol/d. Salt sensitivity, defined as an increase in mean arterial blood pressure >/=3 mm Hg with salt loading, was deemed "moderate" if increasing </=10 mm Hg and "severe" if increasing more. When dietary potassium was 30 mmol/d, salt loading induced a mean increase in blood pressure only in blacks (P<0.001), and salt sensitivity occurred in most blacks but not whites (79% vs 36% (P<0.02). Supplementing potassium only to 70 mmol/d attenuated moderate salt sensitivity similarly in blacks and whites; 120 mmol/d abolished it, attenuated severe salt sensitivity, which occurred in a quarter of affected blacks, and suppressed the frequency and severity of salt sensitivity in blacks to levels similar to those observed in whites. These observations demonstrate that in most normotensive black men but not white men, salt sensitivity occurs when dietary potassium is even marginally deficient but is dose-dependently suppressed when dietary potassium is increased within its normal range. Such suppression might prevent or delay the occurrence of hypertension, particularly in the many blacks, in whom dietary potassium is deficient.
血压正常的盐敏感性是高血压的一种假定前驱状态，在非裔美国人（黑人）中可能相当常见，而在欧裔美国人（白人）中则较少见，但这仅在膳食钾缺乏时出现，而当钾摄入量维持在正常范围内时则不会出现。我们在对38名健康血压正常男性（24名黑人，14名白人）进行的41项代谢控制研究中检验了这一假设，这些男性食用低钠（15 mmol/d）且钾轻度缺乏（30 mmol/d）的基础饮食6周。在最后4周期间，给予氯化钠负荷（250 mmol/d）；在最后3周期间，将钾补充（以碳酸氢钾形式）至中或高正常水平，即70和120 mmol/d。盐敏感性定义为盐负荷后平均动脉血压升高≥3 mmHg，若升高≤10 mmHg则视为“中度”，若升高超过10 mmHg则视为“重度”。当膳食钾为30 mmol/d时，盐负荷仅使黑人的血压平均升高（P<0.001），且大多数黑人出现盐敏感性，而白人未出现（79%对36%，P<0.02）。仅将钾补充至70 mmol/d时，黑人和白人的中度盐敏感性均得到类似程度的减轻；补充至120 mmol/d时则消除了盐敏感性，减轻了重度盐敏感性（四分之一受影响的黑人出现重度盐敏感性），并将黑人盐敏感性的频率和严重程度降低至与白人相似的水平。这些观察结果表明，在大多数血压正常的黑人男性而非白人男性中，当膳食钾即使轻度缺乏时就会出现盐敏感性，但当膳食钾在正常范围内增加时，盐敏感性会呈剂量依赖性受到抑制。这种抑制作用可能预防或延缓高血压发生，尤其在许多膳食钾缺乏的黑人中。
