RENAL EFFECTS OF DIETARY CHLORIDE IN AFRICAN-AMERICANS

我们最近报道，当饮食中钾的摄入量控制在30 mmol/d（在许多非裔美国人（黑人）中并不少见）时，盐敏感性发生在大多数血压正常的黑人中，但在相对少数的血压正常的高加索裔美国人（白人）中，平均而言，黑人更为严重。 在随后的一项研究中，血压正常和轻度高血压的黑人男性摄入的饮食中钾含量略有不足，我们观察到，在那些盐敏感的人中，饮食中的NaCl负荷诱导了肾血管收缩功能障碍，其中肾血流量（RBF）减少，肾血管阻力（RVR）和滤过（FF）增加，肾小球滤过率呈上升趋势。 饮食NaCl引起的平均动脉压的变化与RBF中引起的变化成反比，与RVR和FF中引起的变化成正比。 在那些黑人谁不是盐敏感，肾功能不全，没有观察到NaCl负荷。 由于柠檬酸钠（和其他非氯钠盐）的饮食负荷未能诱导盐敏感性高血压患者的升压反应，因此柠檬酸钠也可能未能诱导血压正常的盐敏感性黑人的肾血管收缩功能障碍。 我们预期这一发现，并将其解释为证据表明，在黑人中诱导的加压作用，NaCl负荷需要诱导肾血管收缩功能障碍，这反过来又需要加载NaCl的Cl-组分。 我们最近报道，在中风倾向的自发性高血压大鼠喂养正常的氯化钠饮食，补充氯化钾引起持续恶化的高血压，肾血管病变和中风，而补充碳酸氢钾有相反的效果。 当这只大鼠是氯化钠负载，补充氯化钾，但不是碳酸氢钾，进一步加剧高血压和肾血管病变，增加中风的频率，并在数小时内诱导减少尿肌酐排泄。 在血压正常和轻度高血压的黑人中，喂食正常的NaCl饮食（150 mmol/d），钾（45 mmol/d）刚刚足够，我们将确定氯化钾和柠檬酸钾（100 mmol/d）补充14天是否有不同的升压和肾血流动力学效应。 我们预计，这两种补充钾盐将诱导血压下降，但较低的RBF和较高的RVR和FF将参加补充氯化钾。 我们将这些发现解释为，尽管伴随血压降低，但KCl的Cl组分可产生肾血管收缩和潜在的肾病效应。

We recently reported that when dietary potassium was controlled at a marginally deficient intake not uncommon in many African- Americans (blacks), 30 mmol/d, salt sensitivity occurred in the majority of normotensive blacks but in relatively few normotensive Caucasian-Americans (whites), and on average was more severe in blacks. In a subsequent study of normotensive and mildly hypertensive black men consuming a diet marginally deficient in potassium, we observed that in those who were salt- sensitive, dietary NaCl loading induced a renal vasoconstrictive dysfunction in which renal blood flow (RBF) decreased, renal vascular resistance (RVR) and filtration (FF) increased, and glomerular filtration rate trended upward. The changes in mean arterial pressure induced by dietary NaCl varied inversely with those induced in RBF and directly with those in RVR and FF. In those blacks who were not salt-sensitive, renal dysfunction was not observed with NaCl loading. Since dietary loading of sodium citrate (and other non-Cl sodium salts) fails to induce a pressor response in patients with salt-sensitive hypertension, sodium citrate might also fail to induce a renal vasoconstrictive dysfunction in normotensive salt-sensitive blacks. We anticipate this finding, and will interpret it as evidence suggesting that the pressor effect induced in blacks by NaCl loading requires the induction of a renal vasoconstrictive dysfunction, which in turn requires the Cl- component of loaded NaCl. We have recently reported that in the stroke-prone spontaneously hypertensive rat fed a normal NaCl diet, supplemental KCl induced a persisting exacerbation of hypertension, renal vasculopathy and strokes, whereas supplemental KHCO3 had opposite effects. When this rat was NaCl-loaded, supplemental KCl, but not KHCO3, further exacerbated hypertension and the renal vasculopathy, increased the frequency of strokes, and within hours induced a reduction in urinary creatinine excretion. In normotensive and mildly hypertensive blacks fed a normal NaCl diet (150mmol/d) just adequate in potassium (45 mmol/d), we will determine whether KCl and K-citrate (100 mmol/d) supplemented for 14 days have differing pressor and renal hemodynamic effects. We anticipate that both supplemented potassium salts will induce a decrease in blood pressure, but that a lower RBF and a higher RVR and FF will attend supplemental KCl. We will interpret such findings as suggesting that the Cl component of KCl can exert a renal vasoconstrictive and potentially renopathic effect despite a concomitant decrease in blood pressure.