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时，大多数血压正常的黑人发生盐敏感性，但相对较少的血压正常的白人美国人（白人）发生盐敏感性，平均而言黑人更严重。在随后的一项研究中，我们观察到在那些盐敏感的黑人男性中，饮食中的NaCl负荷会引起肾血管收缩功能障碍，其中肾血流量（RBF）减少，肾血管阻力（RVR）和滤过率（FF）增加，肾小球滤过率呈上升趋势。NaCl诱导的平均动脉压变化与RBF呈负相关，与RVR和FF呈正相关。在那些对盐不敏感的黑人中，NaCl负荷未观察到肾功能不全。由于饮食负荷柠檬酸钠（和其他非cl钠盐）不能诱导盐敏感性高血压患者的升压反应，柠檬酸钠也可能不能诱导正常血压盐敏感性黑人的肾血管收缩功能障碍。我们预测了这一发现，并将其解释为证据，表明NaCl负载诱导的黑人升压效应需要诱导肾血管收缩功能障碍，而这反过来又需要负载NaCl的Cl-成分。我们最近报道，在有中风倾向的自发性高血压大鼠中，喂食正常NaCl饮食，补充KCl会导致高血压、肾血管病变和中风的持续恶化，而补充KHCO3则有相反的效果。当这只大鼠被nacl负荷时，补充KCl，而不是KHCO3，进一步加重了高血压和肾血管病变，增加了中风的频率，并在数小时内引起尿肌酐排泄减少。在正常和轻度高血压的黑猫中，给予150mmol/d的正常食盐（150mmol/d）和适量的钾（45mmol /d），我们将测定添加KCl和k -柠檬酸盐（100mmol /d） 14天是否有不同的升压和肾血流动力学效应。我们预计，两种补充钾盐都会导致血压下降，但补充KCl会导致RBF降低，RVR和FF升高。我们将这些发现解释为，尽管伴随血压下降，但KCl的Cl成分可以发挥肾血管收缩和潜在的肾脏病变作用。

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.