Adragna N C, Canessa M L, Solomon H, Slater E, Tosteson D C
Hypertension. 1982 Nov-Dec;4(6):795-804. doi: 10.1161/01.hyp.4.6.795.
Alterations in sodium countertransport and cotransport have been reported in red cells of patients with essential hypertension. We have investigated the relationship between these two systems by performing simultaneous measurements of the maximal rates of lithium-sodium (Li1-Na0) countertransport and outward sodium-potassium (Na-K) cotransport in red cells from normotensive and hypertensive subjects. Li1-Na0 countertransport was assayed by measuring the Na0-stimulated Li efflux from cells loaded to contain 10 mmoles Li per liter of cells by incubation in isotonic LiCl. Na-K cotransport was assayed by measuring the furosemide-sensitive component of Na and K efflux into magnesium-sucrose medium from cells loaded by the p-chloromercuribenzene sulfonic acid (PCMBS) procedure to obtain 50 mmoles of both ions per liter of cells. The mean values (+/- SE) for 16 normotensives and 22 hypertensives were (mmole/liter cells x hour): Na countertransport = 0.29 +/- 0.02 vs 0.51 +/- 0.03 (p less than 0.001); Na cotransport = 0.30 +/- 0.03 vs 0.51 +/- 0.05 (p less than 0.005); and K cotransport = 0.34 +/- 0.03 vs 0.60 +/- 0.04 (p less than 0.005). Li1-Na0 countertransport correlated significantly with Na cotransport (r = 0.50, n = 38, p less than 0.005) and K cotransport (r = 0.57, p less than 0.005). This observation suggests that both transport systems are somehow regulated to be more active in this group of hypertensive patients. The increased cotransport in hypertensive patients is also apparent from two other measurements of Na and K fluxes in red cells suspended in Na medium. First, the furosemide-sensitive net Na efflux into Na medium was (mean +/- SE) 0.25 +/- 0.05 in 10 normotensive subjects and 0.50 +/- 0.09 in 12 hypertensive patients. Second, the furosemide-sensitive net K efflux into Na medium was (mean +/- SE) 0.25 +/- 0.04 in 13 normotensive subjects and 0.43 +/- 0.04 in 16 hypertensive patients (p less than 0.005). We conclude that mean values for both Na countertransport and Na-K cotransport are significantly higher in the group of hypertensives than in the group of normal control subjects.
原发性高血压患者红细胞中钠逆向转运和协同转运的改变已有报道。我们通过同时测量正常血压和高血压受试者红细胞中锂 - 钠(Li1 - Na0)逆向转运的最大速率和外向钠 - 钾(Na - K)协同转运,研究了这两个系统之间的关系。Li1 - Na0逆向转运通过测量在等渗LiCl中孵育至每升细胞含10毫摩尔Li的细胞中,由Na0刺激的Li外流来测定。Na - K协同转运通过测量从经对氯汞苯磺酸(PCMBS)处理加载至每升细胞含50毫摩尔两种离子的细胞中,呋塞米敏感的Na和K外流成分进入镁 - 蔗糖培养基的情况来测定。16名正常血压者和22名高血压者的平均值(±标准误)为(毫摩尔/升细胞×小时):钠逆向转运 = 0.29 ± 0.02 对比 0.51 ± 0.03(p < 0.001);钠协同转运 = 0.30 ± 0.03 对比 0.51 ± 0.05(p < 0.005);钾协同转运 = 0.34 ± 0.03 对比 0.60 ± 0.04(p < 0.005)。Li1 - Na0逆向转运与钠协同转运显著相关(r = 0.50,n = 38,p < 0.005),与钾协同转运也显著相关(r = 0.57,p < 0.005)。这一观察结果表明,在这组高血压患者中,这两个转运系统在某种程度上被调节得更加活跃。从悬浮于Na培养基中的红细胞的另外两项钠和钾通量测量中,也可明显看出高血压患者协同转运增加。首先,在10名正常血压受试者中,呋塞米敏感的净钠外流进入Na培养基的值为(平均值±标准误)0.25 ± 0.05,在12名高血压患者中为0.50 ± 0.09。其次,在13名正常血压受试者中,呋塞米敏感的净钾外流进入Na培养基的值为(平均值±标准误)0.25 ± 0.04,在16名高血压患者中为0.43 ± 0.04(p < 0.005)。我们得出结论,高血压组中钠逆向转运和钠 - 钾协同转运的平均值显著高于正常对照组。