Schmidlin O, Forman A, Tanaka M, Sebastian A, Morris R C
Department of Medicine, General Clinical Research Center, University of California, San Francisco, CA, USA.
Hypertension. 1999 Feb;33(2):633-9. doi: 10.1161/01.hyp.33.2.633.
In 16 African Americans (blacks, 14 men, 2 women) with average admission mean arterial pressure (MAP, mm Hg) 99.9+/-3.5 (mean+/-SEM), we investigated whether NaCl-induced renal vasoconstriction attends salt sensitivity and, if so, whether supplemental KHCO3 ameliorates both conditions. Throughout a 3-week period under controlled metabolic conditions, all subjects ate diets containing 15 mmol NaCl and 30 mmol potassium (K+) (per 70 kg body wt [BW] per day). Throughout weeks 2 and 3, NaCl was loaded to 250 mmol/d; throughout week 3, dietary K+ was supplemented to 170 mmol/d (KHCO3). On the last day of each study week, we measured renal blood flow (RBF) and glomerular filtration rate (GFR) using renal clearances of PAH and inulin. Ten subjects were salt sensitive (SS) (DeltaMAP >+5%) and 6 salt resistant (SR). In NaCl-loaded SS but not SR subjects, RBF (mL/min/1.73 m2) decreased from 920+/-75 to 828+/-46 (P<0.05); filtration fraction (FF, %) increased from 19. 4+/- to 21.4 (P<0.001); and renal vascular resistance (RVR) (10(3)xmm Hg/[mL/min]) increased from 101+/-8 to 131+/-10 (P<0.001). In all subjects combined, DeltaMAP varied inversely with DeltaRBF (r =-0.57, P=0.02) and directly with DeltaRVR (r = 0.65, P=0.006) and DeltaFF (r = 0.59, P=0.03), but not with MAP before NaCl loading. When supplemental KHCO3 abolished the pressor effect of NaCl in SS subjects, RBF was unaffected but GFR and FF decreased. The results show that in marginally K+-deficient blacks (1) NaCl-induced renal vasoconstrictive dysfunction attends salt sensitivity; (2) the dysfunction varies in extent directly with the NaCl-induced increase in blood pressure (BP); and (3) is complexly affected by supplemented KHCO3, GFR and FF decreasing but RBF not changing. In blacks, NaCl-induced renal vasoconstriction may be a pathogenetic event in salt sensitivity.
在16名非裔美国人（黑人，14名男性，2名女性）中，其平均入院平均动脉压（MAP，毫米汞柱）为99.9±3.5（平均值±标准误），我们研究了氯化钠诱导的肾血管收缩是否与盐敏感性相关，如果是，补充碳酸氢钾是否能改善这两种情况。在为期3周的可控代谢条件下，所有受试者均食用含15毫摩尔氯化钠和30毫摩尔钾（K+）（每70千克体重[BW]每天）的饮食。在第2周和第3周期间，氯化钠摄入量增加至250毫摩尔/天；在第3周期间，饮食中的钾补充至170毫摩尔/天（碳酸氢钾）。在每个研究周的最后一天，我们使用对氨基马尿酸（PAH）和菊粉的肾清除率来测量肾血流量（RBF）和肾小球滤过率（GFR）。10名受试者为盐敏感（SS）（ΔMAP>+5%），6名受试者为盐抵抗（SR）。在摄入氯化钠的SS受试者而非SR受试者中，RBF（毫升/分钟/1.73平方米）从920±75降至828±46（P<0.05）；滤过分数（FF，%）从19.4±增至21.4（P<0.001）；肾血管阻力（RVR）（10³×毫米汞柱/[毫升/分钟]）从101±8增至131±10（P<0.001）。在所有受试者中，ΔMAP与ΔRBF呈负相关（r=-0.57，P=0.02），与ΔRVR和ΔFF呈正相关（r=0.65，P=0.006；r=0.59，P=0.03），但与摄入氯化钠前的MAP无关。当补充碳酸氢钾消除了SS受试者中氯化钠的升压作用时，RBF未受影响，但GFR和FF降低。结果表明，在轻度缺钾的黑人中：（1）氯化钠诱导的肾血管收缩功能障碍与盐敏感性相关；（2）该功能障碍的程度与氯化钠诱导的血压（BP）升高直接相关；（3）受补充碳酸氢钾的复杂影响，GFR和FF降低，但RBF不变。在黑人中，氯化钠诱导的肾血管收缩可能是盐敏感性的致病因素。
