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Impaired renal sodium excretion causes sodium retention, which prevents the nocturnal dip in blood pressure (BP); thus, high BP persists until excess sodium is excreted. The authors defined "dipping time" (DT) as the duration until the nocturnal BP falls below 90% of the daytime average. Diuretic (e.g., hydrochlorothiazide [HCTZ]) and angiotensin receptor blocker (ARB) are able to eliminate sodium retention and restore the non-dipper BP rhythm. Reanalysis of two previous studies demonstrate that HCTZ and ARB shortened the DT. Shortening DT correlated directly with the increase in daytime urinary sodium excretion (Study 2). DT can be used as a preliminary indicator of sodium retention.

Recently, we found that an angiotensin II receptor blocker (ARB) restored the circadian rhythm of the blood pressure (BP) from a nondipper to a dipper pattern, similar to that achieved with sodium intake restriction and diuretics (Fukuda M, Yamanaka T, Mizuno M, Motokawa M, Shirasawa Y, Miyagi S, Nishio T, Yoshida A, Kimura G. J Hypertens 26: 583-588, 2008). ARB enhanced natriuresis during the day, while BP was markedly lower during the night, resulting in the dipper pattern. In the present study, we examined whether the suppression of tubular sodium reabsorption, similar to the action of diuretics, was the mechanism by which ARB normalized the circadian BP rhythm. BP and glomerulotubular balance were compared in 41 patients with chronic kidney disease before and during ARB treatment with olmesartan once a day in the morning for 8 wk. ARB increased natriuresis (sodium excretion rate; U(Na)V) during the day (4.5 ± 2.2 to 5.5 ± 2.1 mmol/h, P = 0.002), while it had no effect during the night (4.3 ± 2.0 to 3.8 ± 1.6 mmol/h, P = 0.1). The night/day ratios of both BP and U(Na)V were decreased. The decrease in the night/day ratio of BP correlated with the increase in the daytime U(Na)V (r = 0.42, P = 0.006). Throughout the whole day, the glomerular filtration rate (P = 0.0006) and tubular sodium reabsorption (P = 0.0005) were both reduced significantly by ARB, although U(Na)V remained constant (107 ± 45 vs. 118 ± 36 mmol/day, P = 0.07). These findings indicate that the suppression of tubular sodium reabsorption, showing a resemblance to the action of diuretics, is the primary mechanism by which ARB can shift the circadian BP rhythm into a dipper pattern.

In clinical nephrology, the glomerular filtration rate (GFR) has been recognized as the golden standard to assess renal function. However, a normal GFR does not necessarily mean normal filtration capability of the kidneys, because impaired filtration capability can be compensated for by elevating glomerular hydraulic pressure. Therefore, an early phase of glomerular dysfunction cannot be detected by the baseline GFR alone. On the other hand, glomerular capillary hypertension is widely recognized as one of the strong risk factors for the progression of nephropathies. Now, it is very important to imagine glomerular hemodynamics in each patient with nephropathy for detecting early dysfunction, as well as for evaluating risk factors. Here, I would like to summarize the current status of how an early phase of renal dysfunction can be detected in clinical practice. I truly anticipate that new methods to assess glomerular hemodynamics in humans will be developed in the near future.

Blood pressure-lowering mechanisms of the Dietary Approaches to Stop Hypertension (DASH) diet, rich in fruits, vegetables, and low-fat dairy foods, were analyzed based on the pressure-natriuresis relationship. Participants (n=375) were randomly assigned to control or DASH diet groups by using a parallel-group design. They then ate their assigned diet for 3 consecutive 30-day intervention feeding periods, during which sodium intake varied among 3 levels by a randomly assigned sequence. Urinary sodium excretion rate and mean arterial pressure were measured at the end of each sodium intake level. Mean arterial pressure and urinary sodium excretion were plotted on x and y axes, respectively, for participants eating control and DASH diets and were modeled as linear relationships for simplicity to allow the estimation of the extrapolated x-intercept and slope of the relationships. The DASH diet steepened the slope of the relationship (29.5+/-3.4 vs 64.9+/-13.1 [mmol/d]/mm Hg, P=0.0002) without significantly shifting the x-intercept (94.1+/-0.5 vs 93.2+/-0.6 mm Hg, NS) of the relationship. These data suggest a natriuretic action of the DASH diet.

Recently we found that, in non-dipper type of essential hypertensive patients who showed the lack of nocturnal fall in blood pressure, circadian rhythm of urinary sodium excretion rate was disturbed. In the present study we examined whether postural change in natriuresis is also disturbed in non-dippers. Sixteen inpatients with essential hypertension were maintained on a relatively high sodium diet containing 10 to 12 g of NaCl per day for 8 days. On the 7th day of the study period, 24-h ambulatory blood pressures were measured, and 5-7th days urinary samples were collected for both daytime and night-time. On the last day of the study period, patients stood for 2 h and then lay down for 2 h. Urinary volume and excretion rates of creatinine and sodium were measured every hour in both positions. Night-time urinary sodium excretion rate was significantly higher in non-dippers (n = 9) than that in dippers (n = 7). Night/day ratio of mean arterial pressure had a positive relationship with night/day ratio of urinary sodium excretion rate. In non-dippers, but not in dippers, the mean value of U(Na)V during upright position was significantly lower than that during supine position. There was a significantly negative relationship between upright/supine ratio of U(Na)V and night/day ratio of MAP or night/day ratio of U(Na)V. In patients with non-dipper type of essential hypertension, both natriuresis patterns, circadian rhythm and postural change, were disturbed.

We recently showed that cardiovascular morbidity was higher in sodium sensitive type of essential hypertension than in the non-sodium sensitive type. It was examined whether sodium sensitivity was associated with insulin resistance, an important atherosclerotic cardiovascular risk factor in essential hypertension. Fifty-three patients with essential hypertension, who had normal (n = 12) and impaired (n = 41) glucose tolerance, were placed on high (12-15 g NaCl/day) and low (1-3 g) sodium diets for 1 week each to determine sodium sensitivity. Fasting plasma glucose and insulin concentrations were measured on a regular sodium diet. The homeostasis model assessment insulin resistance index (fasting glucose [mmol/L] x fasting insulin [mU/L]/22.5) was 1.40+/-0.10 and 1.47+/-0.14 in non-sodium sensitive and sodium sensitive groups. The insulin resistance index was positively correlated with the sodium sensitivity index, while was negatively correlated with fractional excretion of sodium (FE(Na)) obtained during a high sodium diet. In addition, the insulin resistance index had a positive relationship with overall creatinine clearance. Sodium sensitivity index was also negatively correlated with FE(Na) obtained during a high sodium diet. These results showed that insulin resistance might participate in the genesis of sodium sensitivity in essential hypertension by enhancing tubular sodium reabsorption, as reflected in decreased FE(Na) and augmented creatinine clearance. Insulin resistance seemed elevated in sodium sensitive state of essential hypertension, leading to future cardiovascular events.

We investigated the relationship between sodium sensitivity and diurnal variation of blood pressure in patients with essential hypertension. Twenty-eight inpatients with essential hypertension were maintained on high sodium (12 to 15 g NaCl per day) and low sodium (1 to 3 g NaCl per day) diets for 1 week each. Twenty-four-hour blood pressure and urinary sodium excretion were measured at the end of each diet period, and the sodium sensitivity index was calculated as the ratio of the change in mean arterial pressure to the change in urinary sodium excretion rate by sodium restriction. Patients whose average mean arterial pressure was lowered more than 10% by sodium restriction were assigned to the sodium-sensitive group (n = 16); the remaining patients, whose mean arterial pressure was lowered by less than 10%, were assigned to the non-sodium-sensitive group (n = 12). In the non-sodium-sensitive group, mean arterial pressure and heart rate fell during the nighttime, and average values of systolic, diastolic, and mean arterial pressures during the night were significantly lower than those during the day during both low and high sodium diets. On the other hand, in the sodium-sensitive group, there was no nocturnal fall in mean arterial pressure, and none of the systolic, diastolic, and mean arterial pressure values during the nighttime was different from the respective pressure values during the daytime during either sodium diet. The sodium sensitivity index was positively correlated with the fall in mean arterial pressure during the nighttime during a high sodium diet (r = .55, P < .01). These results indicate that in patients with sodium-sensitive essential hypertension, blood pressure fails to fall during the night. High sodium sensitivity may be a marker of greater risk of renal and cardiovascular complications, as has been found in nondippers, patients whose blood pressure fails to fall during the night.

It has been postulated that glomerular capillary pressure is elevated in sodium-sensitive types of hypertension. In addition, the presence or absence of renal function reserve, in response to a chronic protein load, is thought to be useful in predicting the existence of glomerular hypertension. Intrarenal hemodynamic parameters in the sodium-sensitive type of essential hypertension were therefore calculated by analyzing the pressure-natriuresis curve, and the preservation of renal function reserve was evaluated. Fifteen patients with essential hypertension were maintained on a normal sodium diet for 1 week and a low-sodium diet for a second week in study 1. This protocol was repeated for low and high protein intake in 8 patients in study 2. Subjects in study 1 whose mean arterial pressure was reduced by more than 10% by sodium restriction were considered sodium sensitive (n = 7), with the remaining patients classified as non-sodium sensitive (n = 8). There were no significant differences in mean arterial pressure (125 +/- 2 mm Hg), glomerular filtration rate (80 +/- 3 ml/min), or renal plasma flow rate (355 +/- 24 ml/min) on the normal sodium diet between sodium-sensitive and non-sodium-sensitive patients. Glomerular capillary pressure (59 +/- 2 mm Hg vs 47 +/- 1 mm Hg, p < 0.0002) was estimated to be elevated in sodium-sensitive patients relative to that in non-sodium-sensitive patients, whereas the whole kidney ultrafiltration coefficient of glomerular capillary walls (0.068 +/- 0.009 (ml/sec)/mm Hg vs 0.221 +/- 0.042 (ml/sec)/mm Hg, p < 0.005) was decreased. Chronic protein loading increased both glomerular filtration and renal plasma flow rates in study 2. Although the sodium sensitivity of blood pressure showed no significant correlation with the increase in either glomerular filtration or renal plasma flow rate, it showed a weak negative correlation with the increase in filtration fraction (r = -0.69, p < 0.06), which is the ratio of the two rates. Taken together, these results suggest that glomerular capillary pressure is elevated and renal function reserve is impaired in patients with sodium-sensitive essential hypertension.

Objective: To examine the acute effects of alcohol on blood pressure and erythrocyte cation concentrations in patients with essential hypertension., Design: An alcoholic drink or an isocaloric control drink was given during supper in random order on different days, and blood pressure and erythrocyte cation concentrations were measured before and 2 h after the meal., Methods: The subjects were 21 men with essential hypertension who habitually drank alcohol. Blood pressure was measured with a semi-automated sphygmomanometer, and erythrocyte cation concentrations were measured by flame photometry after haemolysis with distilled water., Results: Blood pressure decreased after both drinks, but the decrease was significantly larger after the alcoholic drink than after the control drink. There was a significant difference between the changes in erythrocyte sodium caused by the alcoholic and the control drink. Furthermore, there were significant positive correlations between the fall in blood pressures and the decrease in erythrocyte sodium concentration., Conclusion: The predominant acute effect of alcohol ingestion in patients with hypertension is blood pressure reduction, and it may be associated with a decrease in intracellular sodium.

1. The effects of dietary sodium on blood pressure and levels of sodium, other electrolytes and noradrenaline (NA) in the cerebrospinal fluid (CSF) and blood of 15 patients with essential hypertension were studied. The CSF and blood sampling was carried out after 7 days of a high salt intake (16-18 g/day) and after 7 days of a low salt intake (1-3 g/day). 2. Blood pressure and sodium concentrations in CSF and serum were significantly higher in the high salt period than the low salt period (CSF Na+ concentration: 147.7 +/- 0.4 mmol/L vs 145.3 +/- 0.5 mmol/L; P less than 0.001). Levels of CSF pressure and potassium or calcium concentrations were not different between the two periods. Plasma NA and plasma renin activity (PRA) were lower and CSF NA levels tended to be lower in the high salt period. 3. The levels and the changes in sodium and NA in CSF were not significantly different between the salt-sensitive (n = 8) and the non-salt-sensitive (n = 7) subjects, but the changes in plasma NA and PRA were smaller in the salt-sensitive subjects. 4. These results indicate that the sympathetic nervous system is less suppressed in salt-sensitive subjects during high salt intake. This may be due to altered neural responsiveness to sodium loading rather than being greater increases in sodium concentration in the central nervous system.

The differences between sodium sensitive and sodium retaining hypertension were theoretically considered using a water tank model of body fluid volume-blood pressure regulation. If an outlet valve is attached to a tank with a base area corresponding to the reciprocal of total peripheral resistance (TPR) and water is poured into this tank at a rate corresponding to the amount of Na+ intake, then equilibrium should be achieved at a certain water level, volume and output from the outlet, which represent mean arterial pressure (MAP), cardiac output (CO) and urinary Na+ excretion. The height of the outlet from the tank bottom and the size cross-sectional area, of the outlet correspond to the x-intercept and slope of the renal function (pressure-natriuresis) curve, respectively. In both nonsodium sensitive hypertension, due to the shift of the curve toward a higher blood pressure level (elevated height of the outlet) without change in the slope (size of the outlet), and sodium sensitive hypertension, due to the depressed slope of the curve (reduced outlet size), not only MAP (water level) but also CO (water volume) are increased, resulting in sodium retaining hypertension, if TPR (reciprocal of base area) remained unchanged, while CO is relatively unchanged, resulting in nonsodium retaining hypertension, if TPR is elevated. Thus, the MAP and its sensitivity to sodium intake is determined by the renal function curve. Since body fluid volume is determined by both the renal function curve and TPR, however, changes in TPR during the development of hypertension is a major factor in determining whether or not the body fluid volume has to change only a small amount or a large amount. Therefore, the sodium sensitivity of blood pressure and sodium retention must be considered separately.

Blood pressure (BP) becomes more sodium and body fluid sensitive as renal function deteriorates. Thus, hypertension in chronic renal failure is mostly of the sodium sensitive type. We studied whether the increased sodium sensitivity (SS) can be restored to normal on the maintenance phase of hemodialysis (HD) therapy. Body weight (BW) and BP (specifically, mean arterial pressure [MAP]) were measured after HD and before the next HD, and the body fluid sensitivity (BFS) was calculated as the ratio of changes in these factors on both introduction and maintenance phases in HD patients (n = 56) who were not taking any antihypertensive drugs (BFS = delta MAP/delta BW). In a preliminary study, the amount of interdialytic sodium intake (QNa+) was measured (n = 30), and SS was calculated as the ratio of the change in MAP to QNa+ (SS = delta MAP/QNa+). Interdialytic BW gain (3.1 +/- 0.1 kg) was correlated with the amount of sodium intake (136 +/- 17 mEq), resulting in a positive relationship between BFS and SS (r = 0.79, P less than .0001). Therefore, BFS was used as an index of SS. As a whole, BFS decreased from the introduction to the maintenance phase (6.5 +/- 1.0 to 3.5 +/- 0.6 mm Hg/L, P less than .01). This decrease was marked (6.2 +/- 1.1 to 2.9 +/- 0.6 mm Hg/L, P less than .01) in patients (n = 46) whose BP was normalized in the maintenance phase, while not significant (7.9 +/- 1.9 to 6.3 +/- 1.3 mm Hg/L) in patients (n = 10) whose BP was still high.(ABSTRACT TRUNCATED AT 250 WORDS)

We investigated the possible role of renal prostaglandin (PG) E2 in natriuresis associated with supraventricular tachycardia (SVT). In five female patients with paroxysmal tachycardia, SVT was artificially induced and then stopped 60 min later. Before, during, and after SVT, plasma levels of arginine vasopressin and atrial natriuretic peptide (ANP) and the urinary excretion of sodium and PGE2 were measured. Polyuria was observed during SVT. However, natriuresis did not occur until immediately after the termination of SVT. During SVT, the plasma levels of arginine vasopressin tended to decrease. When SVT was terminated, the vasopressin levels increased significantly (p less than 0.01). Urinary excretion of PGE2 tended to decrease during SVT and then increased significantly (p less than 0.01) after SVT ended. Urinary excretion of sodium was correlated (r = 0.699, p less than 0.001) with the urinary excretion of PGE2. Plasma ANP increased during SVT, but there was no correlation with urinary sodium excretion. These results suggest that renal PGE2, the biosynthesis of which may be stimulated by a increase in plasma vasopressin, is an important factor contributing to the natriuresis observed after the end of SVT.

Changes in the serum Na+ concentration and transcellular body fluid distribution during the interdialytic period were simulated as functions of body weight gain assuming that the effective extracellular osmolality consists only of sodium. Our model shows that these changes are mainly determined by the relative ratio between sodium intake and weight gain in this period. If the sodium intake-to-net fluid intake ratio is equal to the postdialytic serum [Na+], neither changes in serum [Na+] nor transcellular fluid shifts occur. When sodium intake is relatively greater than the net water intake, serum [Na+] is increased and transcellular fluid shifts will occur out of the cells. On the other hand, when the net water intake is relatively greater than the sodium intake, serum [Na+] is decreased and fluid is distributed to both the intracellular and extracellular compartments. The combined application of our models for both the intradialytic interval described previously and the interdialytic interval described here is very useful in quantitatively analyzing the overall sodium and water metabolism in dialyzed patients.

The postdialysis levels of serum sodium concentration, urea concentration, and osmolality, as well as the magnitude of both transcellular fluid shifts and sodium removal, were predicted based on computer modeling without measuring body fluid volumes. A 4-h hemodialysis was performed in five patients at a constant ultrafiltration rate of 0.5 L/h using dialysate with normal (141 mEq/L) or high (150 mEq/L) Na+ concentration. The serum sodium concentration, urea concentration, and osmolality, as well as intracellular and extracellular fluid volumes, were determined before and after hemodialysis. The model predictions without measurement of body fluid volumes were in excellent agreement with measured values, suggesting clinical validity. The model may be useful in clinical practice to control the postdialysis levels of sodium and water content by computerized hemodialysis.

To study the aggregation, adhesion, and specific binding of an alpha 2-antagonist, [3H]rauwolscine, to the platelet membrane fractions, platelets were obtained from 30 patients with essential hypertension and nine normotensive subjects fed a high sodium diet (NaCl, 16-18 g/day) for 7 days and thereafter a low sodium diet (NaCl, 1-3 g/day) for 7 days. The patients with essential hypertension were classified as either salt responders (all those who had greater than 7% decrease in mean arterial pressure from the high to low sodium period) or salt nonresponders (all others). In salt responders, the number of alpha 2-adrenergic receptors on platelet membrane fraction was increased from 523.4 +/- 55.4 fmol/mg of protein in the high sodium period to 669.4 +/- 84.0 fmol/mg of protein in the low sodium period (p less than 0.01), whereas it did not change in salt nonresponders. In contrast, the epinephrine-induced platelet aggregation through alpha 2-adrenergic receptors was decreased in nonresponders, from 47.3 +/- 7.4% in the high sodium period to 24.5 +/- 9.3% in the low sodium period (p less than 0.05), while it did not change in responders. No significant change in the number of alpha 2-adrenergic receptors or epinephrine-induced platelet aggregation was observed in the normotensive subjects.

A computer-based model has been developed to predict the changes in serum sodium, urea concentration, and osmolality as well as transcellular fluid distribution which occur during hemodialysis. Sodium and urea transfers across the dialyzer membrane and transcellular fluid shifts in response to the sodium transfer were modeled assuming that only sodium and its accompanying anions are important as effective osmotic substances in extracellular fluid. Model predictions were consistent with values measured in five patients who were studied on hemodialysis at three different dialysate sodium concentrations equal to 7% below and 7% above the predialysis serum concentration. The measurements and model predictions indicate that serum sodium concentration decreases and intracellular fluid volume increases in dialyses with dialysate Na+ concentration used in conventional hemodialysis, whereas serum sodium concentration increases and intracellular volume decreases in high sodium dialyses. An analysis of model predictions indicates that a reasonable estimation of total body water and the intracellular to extracellular volume ratio enables us to accurately predict the magnitude of transcellular fluid shifts induced by hemodialysis as well as the postdialysis serum sodium concentration and osmolality.

The amount of sodium removed by hemodialysis was estimated, without using radioisotopes, as the change in total osmotically active cations, which is the product of the serum sodium concentration and urea-space. The extracellular and total body fluid volumes were measured using 35SO4 and 3H2O, respectively, in five stable hemodialysis patients under four different conditions. Urea-space determined, based on urea kinetics, was consistent with total body fluid volume measured by 3H2O. The amount of sodium removal, estimated as the change in the product of the serum (Na+) and urea-space, was equal to the change in the sodium content, which is the product of the serum (Na+) and extracellular fluid volume measured by 35SO4. Sodium removal may be divided into two components, diffusion and ultrafiltration.

Net Na+ and K+ fluxes were measured in Na+-loaded red cells from 19 normotensive control subjects, 22 essential hypertensive patients, and 8 secondary hypertensive patients. The ratio of Na+/K+ net fluxes was significantly lower in essential hypertensive patients than in normotensive control subjects. However, by the addition of the patients' own plasma, the net Na+ efflux rate was significantly increased in essential hypertensive patients, which caused the increment in the ratio of Na+/K+ net fluxes. This resulted in disappearance of the difference between normotensive and hypertensive subjects in the ratio of cation fluxes. It was possible that the abnormalities of cation transport in red cells from essential hypertensive patients might be compensated for by humoral factors in the plasma.

The dependence of intracellular Na+ activity on the electrical driving force across the luminal membrane and the presence of Cl- in the luminal perfusate was studied in Necturus proximal tubule. Intracellular Na+ and K+ activities were measured with microelectrodes filled with liquid ion exchanger. Perfusion of the tubule lumen with a NaCl-free solution caused cell Na+ activity to fall from the control value of 29.7 to 6.6 mM. In the absence of luminal driving force across the luminal membrane in accordance with simple diffusion of Na+ across this membrane. When the tubule lumen contained Na+ and Cl-, an electrically neutral component of Na+ entry into cells from the lumen appeared in addition to the diffusional component of Na+ entry.

Red cell sodium (RBC-Na+) concentrations were measured using 23Na nuclear magnetic resonance (NMR), without the destruction of erythrocyte membranes. Subjects were categorized into four groups: 20 normotensive subjects (NT group), 20 age-matched essential hypertensive patients (EHT group), 10 patients with primary aldosteronism (PA group), and 18 patients treated with digoxin (DIG group). Although RBC-Na+ concentrations were similar between the NT group (6.14 +/- 0.80 (Mean +/- SD) mmol/l) and the EHT group (5.92 +/- 0.99), they were significantly higher in both the PA group (7.55 +/- 0.88, p less than 0.001) and the DIG group (8.43 +/- 3.81, p less than 0.02). In the PA group, RBC-Na+ concentrations decreased significantly after resection of the adenoma, and there was an inverse relationship between serum potassium and RBC-Na+ concentrations (r = -0.65, p less than 0.01). In the DIG group, RBC-Na+ concentrations tended to increase in proportion to serum digoxin levels (r = 0.53, p less than 0.05). These results support the view that RBC-Na+ concentrations are determined primarily by Na+/K+-pump activity of red cell membranes. This study showed also that Na+ NMR is an useful method determining intracellular Na+ concentrations.

Plasma concentrations of immunoreactive (IR)-atrial natriuretic polypeptide (hANP) were measured by radioimmunoassay in 9 essential hypertensive patients after alteration of salt intake and acute saline infusion. Daily salt intake was altered every one week in the order of 15g/day, 3g/day, and 7g/day. On the last day of the first week, 1500 ml of 0.9% saline was infused intravenously over one hour. Plasma concentrations of IR-hANP tended to decrease, although not significant, by salt restriction. Further, there were significant positive correlations between changes in plasma concentrations of IR-hANP and those of several variables such as body weight, systolic blood pressure, and creatinine clearance. Plasma concentrations of IR-hANP rose significantly (p less than 0.05) from 50.7 +/- 20.1 (Mean +/- SEM) pg/ml to 119.0 +/- 48.8 after acute saline infusion. Although there was significant correlation between mean blood pressure and the increase in sodium excretion by saline infusion, this increase was unrelated to the rise in plasma concentrations of IR-hANP. These results suggest that the release of ANP is stimulated mainly by expansion of extracellular fluid volume in hypertensive patients. However, natriuretic and hypotensive effects attributable to the changes of ANP release could not be elucidated.

This study was performed to determine whether there is any difference in cation transport of red blood cells from normotensive subjects and hypertensive patients in Japan. Net Na+ efflux and net K+ influx rates were measured in sodium-loaded red cells from 19 normotensive subjects, 22 essential hypertensive patients, and 8 secondary hypertensive patients. The ratio of Na+/K+ net fluxes and the net cation flux rate were compared between these groups. The ratio of Na+/K+ net fluxes was significantly lower in essential hypertensive patients than in normotensive subjects. Parameters such as age, sex, blood pressure, plasma renin activity, and plasma aldosterone concentration were also examined in 2 groups of essential hypertensive patients, divided on the basis of their Na+/K+ net fluxes. However, there is no significant difference between the groups. These results suggest that the ratio of cation flux is related to hypertension independently of these parameters.

The present study investigated factors that modify or affect arterial stiffness as assessed by brachial-ankle pulse wave velocity (baPWV) in the general population. Subjects had previously participated in a physical checkup program (n=911), and baPWV and urinary albumin and sodium excretion were also measured. Urine albumin was expressed as the ratio of urine albumin to urine creatinine. Individual salt intake was assessed by estimating 24-h urinary salt excretion and expressed as the ratio of estimated salt intake to body weight. The mean blood pressure and baPWV were 127.1±15.2/77.0±9.5 mm Hg and 15.9±3.3 m s−1, respectively. Univariate analysis demonstrated that baPWV correlated with various factors including age, blood pressure, electrocardiogram voltage (SV1+RV5), urine albumin and salt intake. Multivariate regression analysis revealed that electrocardiogram voltage (P<0.001), systolic blood pressure (P<0.0001), urine albumin (P<0.001) and salt intake (P<0.001), independently correlated with baPWV after adjustment for other possible factors. Similar results were obtained for participants not taking any medication. These results suggest that the baPWV value is independently associated with individual salt intake and cardiac and renal damage, and could be a useful procedure for identifying individuals with concealed risk of cardiovascular disease. [ABSTRACT FROM AUTHOR]