Moderate potassium chloride supplementation in essential hypertension: is it additive to moderate sodium restriction?

Twenty patients with mild or moderate essential hypertension and not receiving any drug treatment, who had been moderately restricting their sodium intake to around 70 mmol(mEq) a day for at least one month and whose mean blood pressure was then 163/103 mm Hg, were entered into a double blind, randomised crossover study to compare one month's treatment with slow release potassium chloride tablets (64 mmol potassium chloride a day) with one month's treatment with a matching placebo. Mean (SEM) urinary sodium excretion on entry to the study was 68 (6.8) mmol/24 h. Mean urinary potassium excretion increased from 67 (6.9) mmol(mEq)/24 h with placebo to 117 (4.6) mmol/24 h with potassium chloride. Supine and standing systolic and diastolic blood pressures did not change significantly with potassium chloride supplementation when compared with pressures while receiving placebo or before randomisation. In patients who are able moderately to restrict their sodium intake doubling potassium as a chloride salt has little or no effect on blood pressure.     

Moderate sodium restriction with angiotensin converting enzyme inhibitor in essential hypertension: a double blind study

Fifteen unselected patients who had essential hypertension and whose average supine blood pressure when they were not receiving any treatment and their usual sodium intake was 162/107 mm Hg were treated with captopril 50 mg twice daily. After one month's treatment their supine blood pressure had decreased to 149/94 mm Hg. They were then instructed to reduce their sodium intake to about 80 mmol(mEq)/day. After two weeks of moderate sodium restriction they were entered into a double blind randomised crossover study comparing the effect of 10 Slow Sodium tablets (100 mmol sodium chloride) with matching placebo tablets while continuing to take captopril and restrict sodium in their diet. After one month of taking placebo their mean supine blood pressure was 137/88 mm Hg with a urinary sodium excretion of 83 mmol/24 h, while after one month of taking Slow Sodium tablets their mean supine blood pressure was 150/97 mm Hg (p less than 0.001) with a sodium excretion of 183 mmol/24 h. The mean supine blood pressure during moderate sodium restriction therefore decreased by 9% and correlated significantly with the reduction in urinary sodium excretion. These results suggest that the combination of treatment with a moderate but practical reduction in sodium intake and an angiotensin converting enzyme inhibitor is effective in decreasing the blood pressure in patients with essential hypertension. This combined approach overcomes some of the objections that have been made to salt restriction alone and to converting enzyme inhibitors alone.     

Beta blockade, diuretics, and salt restriction for the management of mild hypertension: a randomised double blind trial

Ninety four patients with mild hypertension (average supine diastolic blood pressure (phase V) 95-110 mm Hg) were allocated at random to receive restriction of dietary sodium (maximum allowed 70 mmol(mEq)/24 h) or a normal diet. In addition, they received in random order 25 mg chlorthalidone, 200 mg metoprolol (slow release), and a fixed combination of these two drugs. Each drug treatment was given for four weeks and alternated with four weeks of placebo. Forty four patients were allocated to sodium restriction (group 1) and 50 to normal diet (group 2). The mean 24 hour urinary sodium excretion in group 1 was 74 (SD 31) mmol(mEq)/24 h, and in group 2 132 (51) mmol/24 h. Compared with the screening blood pressure the average decrement of the supine blood pressure in group 1 was 16.0/8.6 mm Hg with placebo, 21.7/11.5 mm Hg with the diuretic, 28.5/17.8 mm Hg with the beta blocker, and 28.9/18.4 mm Hg with the combined agent; in group 2 these values were 13.3/6.1, 20.3/9.7, 21.3/12.9, and 29.4/16.8 mm Hg, respectively. There was a sharp decrease of the average potassium concentration during chlorthalidone and combination treatment periods (average value 3.3 mmol(mEq)/1). These results suggest that moderate salt restriction used as sole treatment has a limited though demonstrable blood pressure lowering effect but that when it is used as an adjuvant to beta blocker treatment its value is greatly enhanced.     

Dietary sodium and arterial blood pressure: evidence against genetic susceptibility

Thirty five subjects with both parents in the top third of their age specific blood pressure distributions and 31 subjects with both parents in the bottom third of their blood pressure distributions restricted their intake of sodium for eight weeks while taking part in a double blind, randomised crossover trial of supplements of sodium and placebo. A comparison of two periods of four weeks at different intakes of sodium showed no differences in blood pressure in either the groups as a whole or the subgroups who complied best with the diet and tablets. In the compliant subgroups mean urinary sodium excretions were above 120 mmol(mEq) and below 50 mmol/day. The study provides evidence against the hypothesis that people with a family history of high blood pressure are more susceptible in their blood pressure response to dietary sodium.     

Dietary sodium restriction as adjunctive treatment of hypertension

To examine the effect of modest dietary sodium ion restriction in treated hypertensive individuals, we studied 114 hypertensive patients undergoing individualized dietary counseling with a research dietitian to achieve reduction in dietary sodium ion intake. A significant reduction in mean sodium ion intake was achieved after the first of three lessons and was maintained for 30 weeks with no change in potassium ion intake. Significant falls in blood pressure and body weight were observed with no significant correlations noted between the two variables, implying independence of these effects. Individuals compliant with the dietary sodium ion restriction goal (urinary excretion, less than or equal to 80 mmol/d [less than or equal to 80 mEq/24 h]) were more likely to have a reduction in number of medications than those not reaching that goal. Ninety-eight of the 114 patients completed the entire 30 weeks. Patients who dropped out tended to have lower diastolic blood pressures and required fewer medications for blood pressure control than those who completed the 30 weeks. For these reasons, patients in the former group may have been less highly motivated to complete the study. These observations suggest that modest dietary sodium ion restriction is feasible in treated hypertensive patients and that adherence to such a regimen may permit blood pressure control with fewer medications.     

Blood pressure control during weight reduction in obese hypertensive men: separate effects of sodium and energy restriction

The separate and combined effects of dietary energy and sodium restriction on regulation of blood pressure were investigated in 30 middle aged obese men with essential hypertension attending the outpatient department. In group 1 (n = 15) a basal period with no dietary restriction was followed by a period taking an energy reduced diet (5.1 MJ; 1230 kcal), the sodium intake being supplemented and hence unchanged (1:ErSn). In group 2 (n = 15) the basal period preceded a control period with no intervention, which was followed by taking a diet restricted in energy (5.1 MJ; 1220 kcal) and sodium (2:ErSr). During period 1:ErSn there were reductions in heart rate and urinary noradrenaline output but not in systolic or diastolic blood pressure. Body weight decreased by 4.9-11.7 kg and urinary sodium excretion did not change. In period 2:ErSr urinary sodium output was reduced by 81.4 (SEM 17.8) mmol(mEq)/24 h and there was a weight loss of 8.2 (SEM 0.7) kg. Systolic and diastolic blood pressures fell significantly, as did the heart rate and urinary noradrenaline excretion. These results show that in hypertensive obese men a moderate weight reducing diet decreases indices of sympathetic nervous system activity. Reduction of blood pressure to the normotensive range was observed only when there was a concomitant restriction of sodium intake.     

Controlled trial of enalapril in patients with chronic fluid overload undergoing dialysis

About one third of patients receiving dialysis for end stage renal failure have chronic fluid overload despite advice to restrict their oral fluid intake. To investigate the potential of an angiotensin converting enzyme inhibitor in reducing the urge to drink and consequent gain in weight, a double blind, placebo controlled crossover trial of enalapril was conducted in 25 patients receiving dialysis who had fluid overload. The trial comprised a baseline period of four weeks; two periods of treatment, each of four weeks, during which patients received either placebo or enalapril 5 mg twice each week; and a follow up period of four weeks. Five patients withdrew from the trial, one because of an adverse drug reaction to enalapril. A range of biochemical and behavioural variables was measured during the baseline period, at the completion of periods 1 and 2, and during follow up. These variables included gain in weight between dialysis sessions; blood pressure; plasma concentrations of sodium, angiotensin II, and vasopressin; plasma renin and angiotensin converting enzyme activities; osmolality; and estimations of thirst, intake of fluid, and control of drinking. Enalapril caused a significant reduction in gain in weight between dialysis sessions, thirst, and oral intake of fluid in parallel with significantly increased renin activity, significantly decreased angiotensin converting enzyme activity, and decreased concentrations of angiotensin II. Gain in weight and angiotensin converting enzyme activity returned to baseline values once patients stopped taking enalapril. These results suggest that enalapril may act on the renin-angiotensin system and reduce intake of fluid by inhibiting angiotensin converting enzyme.     

Hypokalemia during the treatment of arterial hypertension with diuretics.

In a study of 50 patients with uncomplicated arterial hypertension the administration of hydrochlorothiazide, 50 to 100 mg daily or every other day, with or without reserpine, 0.25 mg daily, resulted in a fall in the mean blood pressure from 182/113 to 144/92 mm Hg. The mean duration of therapy was 19 months. The mean serum potassium concentration was 4.3 mmol/l before the onset of therapy. It fell during the first 6 weeks of treatment, but seldom below 3.5 mmol/l, then rose gradually and spontaneously to 4.1 mmol/l after 19 months of therapy. All the patients remained asymptomatic. These findings bring into question the routine use of potassium supplements or a potassium-sparing diuretic, such as spironolactone or triamterene, during the treatment of hypertension with diuretics such as the thiazides. The use of potassium supplements or a potassium-sparing agent may induce hyperkalemia in spite of the simultaneous administration of a diuretic that acts more proximally. Since hyperkalemia is potentially lethal, the serum potassium concentration should be carefully monitored in any patient receiving potassium supplements or a potassium-sparing agent.     

SODIUM AND POTASSIUM LEVELS IN HYPERTENSIVE CHILDREN

In a baseline survey of 4,936 school children aged 6-16 years, 199 children with systolic blood pressure (SBP) values equal or greater than the 95-th percentiles for age and sex were chosen as the hypertensive group (HBP), and were matched for age and sex with 197 children with SBP from the 5-th through the 50-th percentiles as the control (normotensive) group (NBP). For both groups the intra-RBC and plasma sodium and potassium contents, 8-hour night urinary sodium, potassium and creatinine excretions for three days, and an oral saline-water load test were performed. The results show that (1) intra-RBC potassium level in the HBP was lower than that in NBP. The level in those with positive hypertension family history (FH+) was lower than that with negatives (FH-). The intra-RBC potassium contents correlated inversely with diastolic BP. No correlation between intra-RBC sodium and BP was found; (2) Plasma sodium concentration in HBP was much lower than that in NBP. No difference was found between the FH+ and FH- in the plasma sodium concentrations; (3) Mean 8-hour night urinary potassium excretion expressed as mmol/g creatinine, was lower in HBP than in NBP; (4) After the saline load test the 4-hour urinary sodium excretion was significantly higher in HBP. Of those children with FH- the 4-hour sodium excretion in HBP was higher than that in NBP, but no significant difference was found between HBP and NBP of the FH+ children in the 4-hour urinary sodium excretions.(ABSTRACT TRUNCATED AT 250 WORDS)     

二甲双胍治疗抗精神病药物引起的血脂异常:两项随机、安慰剂的对照研究

目的：验证二甲双胍治疗抗精神病药引起的血脂异常的疗效和安全性。方法：将两项随机、安慰剂的 对照研究纳入分析。共有201例服用抗精神病药物后出现血脂异常的首发精神分裂症患者,并将其分为1 000 mg/d 二甲双胍组(以下简称为二甲双胍组,n=103)和安慰剂组(n=98),观察24周。在基线、治疗后第12周和第24周进行 临床症状及体重、血糖、血脂等代谢指标的评估。结果：二甲双胍治疗后,二甲双胍组和安慰剂组之间低密度脂 蛋白胆固醇(low density lipoprotein cholesterol,LDL-C)的平均差异从基线时的0.16 mmol/L,降低到第24周结束时的 –0.86 mmol/L,降低了1.02 mmol/L,差异有统计学意义(P<0.01)。而24周结束时,二甲双胍组LDL-C≥3.37 mmol/L的 患者有25.3%,显著低于安慰剂组24周结束时的64.8%(P<0.01)。与安慰剂组相比,二甲双胍组的体重、体重指数、 胰岛素、胰岛素抵抗指数、总胆固醇、三酰甘油和高密度脂蛋白胆固醇也有显著变化,差异均有统计学意义(均 P<0.05)。治疗对体重和胰岛素抵抗的影响出现在第12周,并且在第24周进一步改善,但对改善血脂异常的作用在第 24周结束时才出现。结论：二甲双胍治疗对于改善抗精神病药物引起的血脂异常和胰岛素抵抗是有效的,并且改善 抗精神病药物诱导的胰岛素抵抗出现的时间早于降低血脂异常的时间。     

波依定治疗原发性高血压病的疗效评价

为评价波依定(非洛地平缓释片)对原发性高血压痛的疗效。病人在服用安慰剂1用后,将原发性高血压病102例分为波依定组56例,硝苯地平组46例。两组病例均排除继发性高血压病、急进型高血压病、脑血管意外、嗜咯细胞瘤等病人,用随机、双盲方法进行自身对照开放性试验。测量服药后第1、2、4、8周时的血压,进行自身服药前后值的对比。设硝苯地平对照组与波依定对比服药后第1、2周时的血压值。观察服药前后24小时动态血压变化,测T/P比值,并与络合喜T/P值对比。观察服药前后血生化的改变。结果:(1)自身对照开放试验患者在服药后第1、2、4、8周的降压疗效结果:无效17例,有效28例,优36例,佳48例,总显效卑86.71％。(2)波依定组与硝苯地平组对比,1周后波组DBP 12.09±0.97kPa,硝组12.85±1.33kPa(P=0.0031),2周后波组DBP 11.97±0.80kPa,硝组12.66±1.15kPa(P=0.0018)。(3)24小时动态DBPT/P67.72±2.35％,对照组络合喜67％,两组疗效一样,均>50％都有效。(4)服用波依定前后病人血生化对比(P>0.05)无明显差异。结果提示波依定是治疗原发性高血压的有效药物,其疗效好副作用少。     

Effect of aliskiren on arterial stiffness, compared with ramipril in patients with mild to moderate essential hypertension

Background Aliskiren is a novel blood pressure-lowering agent acting as an oral direct renin inhibitor.The aim of this study was to assess the effect of aliskiren on arterial stiffness,compared with th...     

Diuretics, serum and intracellular electrolyte levels, and ventricular arrhythmias in hypertensive men.

OBJECTIVE--To investigate the patterns of electrolyte abnormalities resulting from thiazide administration and whether they cause ventricular arrhythmias, and to help resolve the controversy over whether clinicians should routinely prescribe potassium-conserving therapy to all patients treated with thiazides. DESIGN--Double-blind, randomized controlled trial. PARTICIPANTS--A total of 233 hypertensive men aged 35 to 70 years. INTERVENTIONS--Participants were withdrawn from prior diuretic treatment and were replenished with oral potassium chloride and magnesium oxide. They were then randomized to 2 months of treatment with (1) hydrochlorothiazide; (2) hydrochlorothiazide with oral potassium; (3) hydrochlorothiazide with oral potassium and magnesium; (4) hydrochlorothiazide and triamterene; (5) chlorthalidone; or (6) placebo. MAIN OUTCOME MEASURES--Ventricular arrhythmias on 24-hour Holter monitoring and serum and intracellular potassium and magnesium levels. RESULTS--Of the 233 participants, 212 (91%) completed the study. Serum potassium levels were 0.4 mmol/L lower in the hydrochlorothiazide group than in the placebo group (P less than 0.01), and this mean difference was not affected by supplementation with potassium, with potassium and magnesium, or with triamterene. However, the supplements did prevent the occasional occurrence of marked hypokalemia; all 12 of the men who developed serum potassium levels of 3.0 mmol/L or less were among the 90 who received diuretics without supplementation (P less than 0.01). Similarly, the overall proportion of men with ventricular arrhythmias was not affected by randomized treatment, but there was a twofold increase in the proportion with arrhythmias among the 12 men with serum potassium levels of 3.0 mmol/L or less (P = .02). Serum magnesium and intracellular potassium and magnesium levels were not reduced by hydrochlorothiazide, nor were they related to ventricular arrhythmias. CONCLUSIONS--In the majority of hypertensive patients, treatment with 50 mg/d of hydrochlorothiazide does not cause marked hypokalemia or ventricular arrhythmias. However, because some individuals will develop hypokalemia after starting diuretic therapy, serum potassium levels should be monitored and potassium-sparing strategies should be used when indicated.     

The effects of a high fibre, low fat and low sodium dietary regime on diabetic hypertensive patients of different ethnic groups.

Fifty-three diabetic patients with mild hypertension were allocated to a treatment diet with a high fibre, low fat and low sodium dietary regime or a control diet. After a 1-month treatment period, the modified-diet treated group (n = 35) showed a highly significant reduction in mean diastolic blood pressure (P less than 0.001) accompanied by significant reduction in urinary sodium excretion (P less than 0.01). The mean values of diastolic pressure (P less than 0.05) and urinary sodium/potassium ratio (P less than 0.01) were also significantly reduced at 1 month compared to control. White (n = 16) and West Indian (n = 10) diabetic hypertensive patients demonstrated a similar significant hypotensive response (P less than 0.05 and less than 0.01 respectively) with reduction in urinary sodium excretion to the modified diet. In contrast, Asian patients demonstrated no significant changes. Treatment of hypertension in diabetic subjects with a high fibre, low fat and low sodium dietary regimen may have a hypotensive response after a period of 1 month and there is a similar response in both black and white ethnic groups. Further observation of these patients will determine long-term response and compliance.     

Blood pressure and metabolic effects of calcium supplementation in normotensive white and black men

A randomized, double-blind, placebo-controlled trial was conducted to examine the effect of calcium supplementation on blood pressure in normotensive black (n = 21) and white (n = 54) men, aged 19 to 52 years. After a four-week baseline period of weekly blood pressure measurement, subjects were randomly assigned within racial groups to either a treatment (calcium, 1500 mg/d) or placebo group for a 12-week period. During the experimental period, multiple blood pressure measurements were taken every two weeks in both the seated and supine positions, using a random baseline sphygmomanometer. A repeated-measures analysis of covariance yielded a modest but significantly lower seated mean arterial pressure in the treatment group compared with the control group, but no differences between the races. Results were similar for supine blood pressure. Calcium supplementation, in comparison with placebo, resulted in lower mean arterial pressure in normotensive white and black men during a 12-week period. The overall blood pressure-lowering effect was not correlated with the response of serum levels of total and ionized calcium, total inorganic phosphorus, or parathyroid hormone, or overnight urinary electrolyte values.     

Converting enzyme inhibition and kidney function in normotensive diabetic patients with persistent microalbuminuria

The effects of a long term reduction in blood pressure on the kidney function of normotensive diabetic patients who had persistent microalbuminuria (30-300 mg albumin/24 hours) were studied in two groups of 10 such patients before and during six months of treatment with either 20 mg enalapril or placebo daily. Treatments were assigned randomly in a double blind fashion. Before treatment both groups had similar clinical characteristics, weight, diet, total glycosylated haemoglobin, median albumin excretion rate (enalapril group 124 mg/24 h, placebo group 81 mg/24 h), and mean arterial pressure (enalapril group 100 (SD 8) mm Hg, placebo group 99 (6) mm Hg). During treatment weight, urinary urea excretion, and total glycosylated haemoglobin remained unchanged. The mean arterial pressure decreased in the enalapril group but not in the placebo group (enalapril group 90 (10) mm Hg, placebo group 98 (8) mm Hg). The median albumin excretion rate also fell in the enalapril group but not in the placebo group (enalapril group 37 mg/24 h, placebo group 183 mg/24 h.) The glomerular filtration rate rose in the enalapril group from 130 (23) ml/min/1.73 m2 to 141 (24) ml/min/1.73 m2, and total renal resistances and fractional albumin clearance decreased while fractional albumin clearance increased in the placebo group. These results show that in patients who have diabetes but not hypertension a reduction in blood pressure by inhibition of converting enzyme for six months can reduce persistent microalbuminuria, perhaps by decreasing the intraglomerular pressure.     

Renin predicts diastolic blood pressure response to nonpharmacologic and pharmacologic therapy.

OBJECTIVE--Plasma renin activity was measured at baseline and 6 months in a trial of nonpharmacologic therapy of mild hypertension to determine whether plasma renin activity predicts the diastolic blood pressure (DBP) response to nonpharmacologic therapy. DESIGN, SETTING, AND PARTICIPANTS--Randomized controlled trial of volunteers from the general community with mild hypertension (DBP between 90 and 100 mm Hg), off all antihypertensive therapy at baseline, treated in special research clinics (n = 593). INTERVENTIONS--Subjects were randomly assigned to usual, weight loss, or low sodium/high potassium diet and then randomly assigned to receive placebo, chlorthalidone, or atenolol. MAIN OUTCOME MEASURES--Renin was analyzed as plasma renin activity and as a renin index (logarithm of 24-hour urinary sodium excretion times logarithm of plasma renin activity) (593 patients at baseline and 6 months) to correct for varied sodium intakes. The DBP was measured using the random zero device. RESULTS--Change in DBP at 6 months could be predicted from baseline plasma renin activity or renin index. The DBP was decreased after 6 months of therapy by 2 mm Hg for each unit increase in baseline plasma renin activity and by 0.16 mm Hg for each unit increase in baseline renin index. Patients in the highest renin index quartile had a greater DBP response to atenolol therapy, and patients in the lowest renin index quartile had a greater DBP response to chlorthalidone therapy. Weight loss diet achieved a greater reduction in DBP in patients with higher baseline renin index and had an additive effect on DBP response in both of the drug groups. Patients on a weight loss diet receiving placebo in the highest baseline renin index quartile had a reduction in DBP of 12.4 mm Hg, compared with 4.4 mm Hg in the lowest baseline renin index quartile (P = .009). A low sodium/high potassium diet had a lesser effect than a weight loss diet on pharmacologic therapy. As with the weight loss diet, patients on a low sodium/high potassium diet in the highest baseline renin index quartile had a greater reduction in DBP than patients in the lowest baseline renin index quartile. CONCLUSIONS--These data suggest a significant relationship between baseline levels of plasma renin index and the likelihood of success of nonpharmacologic treatment of hypertension.     

Role of nifedipine in treatment of hypertension

The efficacy of nifedipine in the treatment of hypertension was assessed in 15 patients whose hypertension continued while being treated with atenolol 100 mg and bendrofluazide 5 mg daily. Nifedipine was added in doses of 10, 20, and 30 mg three times daily in a placebo controlled, double blind trial. One patient was withdrawn from the trial because of severe postural hypotension with the highest dose. Erect and supine blood pressure in the remaining 14 patients were significantly reduced by all doses of nifedipine. The drug was well tolerated but plasma potassium fell by 0.3 mmol(mEq)/1 during treatment (p less than 0.05). Nifedipine is thus effective in the treatment of hypertension but should probably be used in combination with a potassium sparing diuretic.     

比索洛尔/氢氯噻嗪复方片对轻、中度原发性高血压患者血压昼夜节律的影响

目的：采用动态血压监测观察比索洛尔/氢氯噻嗪复方片（2.5mg/6.25mg,Lodoz）对轻、中度原发性高血压患者的血压昼夜节律的影响。方法：选择90例收缩压（SBP）〈180mmHg、舒张压（DBP）95～109mmHg的轻、中度原发性高血压患者,口服Lodoz共4周,用24h动态血压监测评价治疗4周后动态血压和血压昼夜节律变化。结果：（1）治疗4周后,“杓型”和“非杓型”组的24hSBP/DBP分别降低9.57/7.75mmHg和12.61/9.88mmHg,日间SBP/DBP分别降低10.59/8.20mmHg和10.91/8.00mmHg,“杓型”和“非杓型”组间的24h和日间SBP/DBP治疗前后差异无统计学意义（P〉0.05）。（2）“杓型”组夜间SBP/DBP降低6.12/5.65mmHg,“非杓型”组降低17.33/13.61mmHg,两组间差异显著（P〈0.01）。（3）“杓型”组的夜间SBP/DBP下降百分比治疗前后无显著性差异（P〉0.05）,血压昼夜曲线仍为“杓型”。“非杓型”组的SBP/DBP夜间下降百分比在治疗后显著增加（P〈0.01）,SBP/DBP的夜间下降百分比两组间比较,差异显著（P〈0.01）。结论：比索洛尔/氢氯噻嗪复方片（2.5mg/6.25mg/d）对“非杓型”组患者的夜间SBP/DBP降低作用较明显,有益于保持正常的血压昼夜节律。     

The urinary sodium: potassium ratio and response to diuretics in resistant oedema.

Nineteen patients with severe oedema due to either cirrhosis of the liver or to congestive cardiac failure, who had failed to respond to previous diuretic therapy, were treated with either increasing doses of frusemide (Group A), or with frusemide in a fixed dose of 80 mg daily and increasing doses of spironolactone (Group B). In Group A there was an inverse correlation between the baseline 24-hr urinary sodium: potassium (Na : K) ratio and the 24-hr urinary potassium excretion during diuresis, and a direct correlation between the urinary Na : K ratio before and after diuresis. Thus, in patients of this group during diuresis, there was a significantly higher urinary potassium excretion in those with a baseline urinary Na : K ratio of less than 1, as compared with those with a ratio of greater than 1. In Group B a satisfactory diuresis was achieved without marked urinary potassium loss in those patients with a baseline urinary Na : K ratio of less than 1, whereas no diuresis was obtained in the two patients with a baseline urinary Na : K ratio of greater than 1. These results suggest that the measurement of the baseline urinary Na : K ratio is of help in determining the potential value of spironolactone in patients with resistant oedema.