Reduced sodium chloride intake normalises blood pressure distribution

The blood pressure distribution of 172 healthy normotensive subjects aged 3-77 years receiving diets containing different amounts of sodium are presented. On their usual intake of sodium (154 +/- 63 mmol Na+/day) and after two weeks on a high sodium intake (201 +/- 92 mmol Na+/day) supine systolic and supine diastolic blood pressure distribution were positively skewed to the right. After two weeks on a reduced sodium diet (77 +/- 37 mmol Na+/day) the blood pressure distribution was normal. An incremental effect of sodium on diastolic blood pressure occurred in 22% of the subjects. The fall in blood pressure on the reduced sodium diet in these 'sodium sensitive' subjects reduced the mean blood pressure level, which was associated with 'normalisation' of the blood pressure distribution.     

The role of sex hormones and sodium intake in postmenopausal hypertension.

To determine the role of sex hormones and sodium intake in hypertension seen in postmenopausal woman, 12 women (aged 50 to 59 years) in whom blood pressure increased for the first time to above 150/90 mmHg after cessation of menstruation were examined in comparison with 7 age-matched postmenopausal normotensive women (118 +/- 2/62 +/- 3 mmHg). All subjects were admitted to the hospital and their sodium intake was maintained at 204 (normal), 306 (high), and 51 (low) mmol/day for 5 days each. In each period, body weight, blood pressure, heart rate, serum levels of sex hormones and vasoactive hormones, and urinary excretions of sodium, kallikrein and dopamine were determined. The plasma levels of prolactin, progesterone, oestrone, and oestradiol in the hypertensive women were all significantly lower than those in the normotensive women in all study periods. With a change in sodium intake from high to low, blood pressure in 8 out of 12 hypertensive patients decreased by more than 10% from 160 +/- 2/100 +/- 2 mmHg to 144 +/- 2/87 +/- 2 mmHg, while in the normotensive women, only 1 out of 7 patients responded to this change in sodium intake. The changes in sodium intake did not alter the plasma levels of sex hormones in the hypertensive and normotensive subjects. Among the hypertensive patients, three had a history of pregnancy-induced hypertension, while none of the normotensive subjects had such a history. The results of the present study suggest that decreases in sex hormones and increased sensitivity to sodium are important factors in the genesis of postmenopausal hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of changes in dietary sodium and potassium on blood pressure and cellular electrolyte handling in young normotensive subjects

In a study on 22 normotensive male subjects, a change in dietary sodium intake from 29.6 +/- 6.0 to 332.5 +/- 13.9 mmol/day (mean +/- s.e.m.), over 7 days, was associated with a significant rise in supine and standing systolic blood pressure and a fall in sodium pump activity. Intracellular sodium remained constant, while intracellular potassium fell. These changes appeared to be reversed by the addition of potassium (96 mmol/day) to the high sodium diet. The 12 subjects with a family history of essential hypertension, as determined by measurement of parental blood pressure, did not differ in their response from those whose parents were normotensive.     

Natriuresis-pressure relationship in polycystic kidney disease

We studied, under outpatient conditions, nine patients with autosomal dominant polycystic kidney disease who were hypertensive on their usual diet, and nine normotensive healthy probands. The subjects were examined in random order on the 7th day after equilibration on a low-sodium diet (20 mmol/day) and again on the 7th day after equilibration on the same diet but with added sodium to yield a final intake of 200 mmol/day (or vice versa). Blood pressure was monitored non-invasively for 2 h at 4-min intervals using an automatic system. In healthy probands, mean arterial pressure (MAP) was similar on the low- and the high-sodium diets (92.7 versus 91.9 mmHg). In hypertensive patients, a significant (P less than 0.02) increase in mean MAP (107.2 versus 111.2 mmHg) and in systolic blood pressure (140.6 versus 148.7 mmHg) was observed irrespective of whether the glomerular filtration rate (GFR) was normal or reduced. The natriuresis pressure curve showed an upward shift (resetting) and a positive slope (sodium sensitivity). Patients with a reduced GFR as shown by inulin clearance differed from probands and patients with a normal GFR, by showing greater proportional changes in GFR and body weight. In hypertensive patients, atrial natriuretic factor (ANF) levels were higher at baseline and showed an exaggerated response to sodium loading. Changes in angiotensin II (Ang II) or in Ang II binding sites on platelets were similar in patients and controls and changed appropriately with the sodium intake. These data show a resetting of the natriuresis-blood pressure relationship and an increased blood pressure sensitivity to sodium in hypertensive patients with adult, dominant, polycystic kidney disease.     

Effects of potassium on sodium balance, renin, noradrenaline and arterial pressure

To determine the effects of potassium on blood pressure and factors affecting blood pressure, we conducted a randomized, placebo controlled trial of a potassium chloride-based substitute for table salt in 23 patients with mild to moderate essential hypertension. In addition, the effects of potassium chloride on sodium balance were studied in 10 normal subjects. Potassium loading with 100 mmol/day over five days in these normal subjects caused a cumulative negative sodium balance of 138 +/- 35 mmol, similar in degree to that achieved by severe dietary sodium restriction. However, two weeks of potassium treatment (100 mmol/day) in patients with essential hypertension did not lower blood pressure (BP) either in the supine or upright positions (potassium treatment: mean BP 108 +/- 3 lying and 113 +/- 3 mmHg standing; placebo treatment: mean BP 109 +/- 3 lying and 115 +/- 3 mmHg standing). Patients found it difficult to tolerate the potassium-based salt substitute in the dose given. We conclude that it is premature to recommend an increase in potassium chloride intake as treatment for raised blood pressure.     

Circadian variation and blood pressure: response to rapid weight loss by hypocaloric hyponatraemic diet in obesity.

Ambulatory intra-arterial blood pressure was monitored in 15 obese hypertensive and 10 obese normotensive subjects weighing more than 30% of their ideal body weight. Measurements were taken before and after 1 month in hospital on a diet of 330kCal/day designed to ensure 34 g protein and 65 mmol sodium. Mean +/- s.d. body mass index in the whole group fell from 40.8 +/- 7.6 to 37.2 +/- 7.4 kg/m2 (P less than 0.0001). Daytime intra-arterial blood pressure fell from 176 +/- 19/102 +/- 14 to 162 +/- 16/95 +/- 14 mmHg (P less than 0.0005 and P less than 0.002) in the hypertensive group and from 141 +/- 15/82 +/- 5 to 131 +/- 13/79 +/- 4 mmHg (P less than 0.005 for systolic pressure) in the normotensive group. Circadian variation of systolic intra-arterial blood pressure comparing the mean daytime with the mean night-time blood pressure recordings showed a day-night difference of 27 +/- 10 mmHg in the normotensive group compared with 12 +/- 13 mmHg in the hypertensive group (P less than 0.01). This trend was reversed after weight loss, when the normotensive group showed a day-night difference of 20 +/- 13 mmHg compared with 18 +/- 17 mmHg in the hypertensive group. Thus, circadian variation of systolic intra-arterial blood pressure in the hypertensive group was significantly (P less than 0.01) reduced compared with the normotensive group prior to, but not after, weight loss. These data show that, in obese subjects, weight loss produced a significant reduction in ambulatory intra-arterial blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

The Effect of Sodium Intake on the Blood Pressure Related to age and Sex

Two hundred and one volunteers with no known hypertension and 60 patients with untreated hypertension were entered into a study that compared the effect of two levels of sodium intake on blood pressure. One hundred and fifty-four volunteers and 46 hypertensive patients reached compliance goals, with a urinary sodium excretion on the high sodium diet twice that on the reduced sodium intake. The blood pressure on the high sodium diet was 4.5 ± 0.5 mmHg (n=154 p > 0.001) higher than on the reduced sodium diet in normotensive individuals and was increased by 8.4 ± 1.5 mmHg (n=46 p > 0.001) in hypertensive individuals. In the volunteer group the major rise in blood pressure occurred in people over the age of 50. In the hypertensive patients the alteration in blood pressure was not age dependent. In the younger age groups some individuals had an increase in blood pressure when on the high sodium intake which was outside the spontaneous variations in blood pressure of a control group. This implied that a number of young normotensive individuals were susceptible to this alteration in sodium intake.

Changes in sodium intake alter blood pressure in hypertensive people, in normotensive people over 50 and in a small number of younger normotensive people. Overall reduction of sodium intake from 200 - 70 mmol/day would reduce the blood pressure level of the population and would reduce the number of people who have a blood pressure that requires drug therapy.     

Regulation of platelet receptors for angiotensin II in man

The effects of changes in dietary intake of sodium and potassium on 125I-angiotensin II binding to platelets were studied in normal subjects. We also defined binding to platelets from patients with essential hypertension and subjects with normal blood pressure. Restriction of sodium intake in normal subjects resulted in a decrease in the number of receptor sites from 6.2 +/- 0.3 sites/cell to 4.1 +/- 0.4 sites/cell (P less than 0.01) but there were no changes in affinity as measured by the Kd. Over a range of sodium intakes from 15 to 200 mmol/day there was a negative correlation between plasma concentration of angiotensin II and receptor site concentration (rs = 0.57, P less than 0.01). Changes in dietary potassium did not affect angiotensin II binding. Angiotensin II binding was also measured in 10 patients with essential hypertension (mean blood pressure [BP] 178/107 mmHg, plasma concentrations of renin [PRC] 12 +/- 2 microU/ml and angiotensin [pANG] II 14 +/- 2 pg/ml) and 10 subjects with normal blood pressure (mean BP 112/74 mmHg, PRC 13 +/- 2 microU/ml, pANG II 13 +/- 2 pg/ml). In the hypertensive patients, binding capacity and affinity (Kd = 5.0 +/- 0.6 X 10(-10) M, 5.7 +/- 0.8 sites/cell) were similar to those in the normotensive subjects (Kd = 4.9 +/- 0.8 X 10(-10) M, 5.4 +/- 0.5 sites/cell). Changes in sensitivity to angiotensin II in essential hypertension may not be determined at receptor level. Angiotensin II receptors in platelets respond to changes in sodium intake like receptors in arterial muscle.     

Plasma atrial natriuretic peptide in young normotensive subjects with a family history of hypertension and in young hypertensive patients

Plasma atrial natriuretic peptide (ANP) behavior was evaluated in 26 untreated essential hypertensives, 21 normotensives, and 20 normotensives with hypertensive heredity under normal sodium intake (120 mEq of Na+/day). All subjects were men, mean age 22.1 +/- 1.9 years. Plasma ANP was evaluated by radioimmunoassay on samples collected in supine position upon waking and again after 1 h of orthostatism. Resulting data showed that ANP in hypertensives (supine = 44.5 +/- 19.4 pg/mL, orthostatism = 24.1 +/- 11.6 pg/mL) was at higher levels than in controls (supine = 38.3 +/- 19.4 pg/mL, orthostatism = 19.9 +/- 10.6 pg/mL) or in normotensives with hypertensive heredity (supine = 42.1 +/- 16.8 pg/mL, orthostatism = 23.2 +/- 10.8 pg/mL). Mean ANP level was higher in the latter group than in the control group (supine = +9%; orthostatism = +14.2%). In conclusion, plasma ANP is raised in young essential hypertensives, resulting in slightly elevated levels in normotensives with hypertensive heredity.     

Effects of dietary sodium on blood pressure in IDDM patients with nephropathy

Summary The objectives of the study were to assess the effects of moderate sodium restriction on blood pressure in insulin-dependent diabetic (IDDM) patients with nephropathy and high normal or mildly hypertensive blood pressure (primary objective), and to document possible associated changes of exchangeable body sodium, body volumes, components of the renin-angiotensin-aldosterone system, atrial natriuretic peptide, and catecholamines (secondary objective). Sixteen patients with untreated systolic blood pressure 140 <160 mmHg and/or diastolic blood pressure 85 <100 mmHg were included in a double-blind, randomized, placebo-controlled trial. After a 4-week run-in period on their usual diet and a 2-week dietary training period to reduce sodium intake to about 90 mmol/day, eight patients received 100 mmol/day sodium supplement (group 2) and eight patients a matching placebo (group 1) for 4 weeks while continuing on the reduced-sodium diet. Patients were examined at weekly intervals. Main response variables were mean values of supine and sitting systolic and diastolic blood pressure as measured in the clinic and by the patients at home. The differences in blood pressure between the beginning and the end of the blinded 4-week study period were calculated and the differences in changes between the two patient groups were regarded as the main outcome parameters. During the blinded 4-week study period, average urinary sodium excretion was 92±33 (mean ± SD) mmol/day in group 1 and 199±52 mmol/day in group 2 (p=0.0002). The differences in blood pressure changes between the two patient groups were 3.9(–1.2 to 9) mmHg [mean (95% confidence intervals)] for systolic home blood pressure, 0.9(–3.7 to 5.5) mmHg for diastolic home blood pressure, 4.9(–3.3 to 13.1) mmHg for clinic systolic blood pressure and 5.3(1 to 9.7 mmHg, p=0.02) for clinic diastolic blood pressure. Combining all patients, there were relevant associations between changes of urinary sodium excretion and blood volume (Spearman correlation coefficient r=0.57), blood pressure and angiotensin II (diastolic: r=–0.7; systolic: r=–0.48), and exchangeable body sodium and renin activity (r=–0.5). In conclusion, in this study of IDDM patients with nephropathy and high normal or mildly hypertensive blood pressure, a difference in sodium intake of about 100 mmol/day for a period of 4 weeks led to a slight reduction of clinic diastolic blood pressure. Studies including larger numbers of patients with various stages of nephropathy and hypertension are needed to definitely clarify the effects of sodium restriction in IDDM.Abbreviations ACE Angiotensin converting enzyme - ANP atrial natriuretic peptide - CV coefficient of variation - GFR glomerular filtration rate - RPF renal plasma flow - PAH paraaminohippuric acid     

Sodium dependence of sodium-proton exchange in platelets from patients with essential hypertension.

The sodium dependence of recovery of cytoplasmic pH (pHi) after an acid load was studied in platelets from 15 patients with untreated essential hypertension (mean arterial pressure 117 +/- 2.3 mmHg, mean +/- SE) and in 15 normotensive controls (mean arterial pressure 90 +/- 2.2 mmHg). Proton flux was measured in gel-filtered platelets loaded with pH sensitive fluorescent indicator. Sodium dependent proton efflux was prevented by 5 (N,N hexamethylene) amiloride, a potent inhibitor of sodium-proton exchange. The relationship between initial rate of proton efflux and extracellular sodium concentration obeyed Michaelis-Menten kinetics. The maximum initial rate of proton efflux was similar in hypertensive and normotensive subjects (1.93 +/- 0.35 mmol H+1/sec, mean +/- SE, and 1.88 +/- 0.26 mmol H+l/sec respectively). The Michaelis-Menten constant (the sodium concentration at which the initial rate of proton efflux is half maximal) was also similar in the two groups: 75.7 +/- 13.9 mmol/l and 8.15 +/- 10.6 mmol/l respectively. There was no significant correlation between either of these parameters and arterial blood pressure.     

Raised plasma levels of atrial natriuretic peptides in Addison's disease

Plasma levels of atrial natriuretic peptides (ANP) were significantly higher in 7 patients with treated Addison's disease (15.8 +/- 8.8 pg/ml, mean +/- SD) than in 7 control subjects (6.1 +/- 3.8 pg/ml) matched for sex, age, body weight and blood pressure. All subjects were studied on their usual sodium intake and had similar urinary sodium excretions. These findings indicate inappropriately high levels of plasma ANP in patients with treated Addison's disease and are possibly due to the lack of adrenal control on ANP synthesis and/or secretion in these patients.     

Two-way factorial study of alcohol and salt restriction in treated hypertensive men

The aim of this study was to determine whether moderate restriction of dietary salt intake leads to an additional fall in blood pressure in treated hypertensive men who are asked to simultaneously reduce their usual alcohol intake. Sixty-three subjects entered an initial 2-week familiarization period during which they continued their usual alcohol intake and commenced a "low sodium" diet (less than 60 mmol/day) supplemented with 100 mmol sodium chloride per day as enteric-coated tablets. Subjects were then randomly assigned to either drink a low alcohol beer alone for a 4-week period (reducing their self-reported alcohol consumption from 537 to 57 ml/week) or to continue their usual alcohol intake (543 versus 557 ml/week). Within the low and normal alcohol intake groups, subjects were assigned to either a low or normal sodium intake. The low sodium groups continued the sodium-restricted diet but were switched to placebo sodium chloride tablets for the 4 weeks. This resulted in a fall in the 24-hour urinary sodium excretion from 144 to 69 mmol/day. The normal sodium groups continued the low sodium diet but kept taking 100 mmol/day of the sodium chloride tablets, and their urinary sodium excretion remained unchanged (125 versus 142 mmol/day). Regular antihypertensive therapy was continued throughout. Fifty-nine subjects completed the trial. In those who reduced their alcohol intake there was a fall in both systolic blood pressure (-5.4 mm Hg supine, p less than 0.01) and diastolic blood pressure (-3.2 mm Hg supine, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Changed cyclic guanosine monophosphate atrial natriuretic factor relationship in hypertensive man

Plasma concentrations of atrial natriuretic factor (ANF) and cyclic guanosine monophosphate (cGMP) were measured in 10 patients with essential hypertension and 10 normotensive controls on the fifth day of a low (50 mmol/day), a medium (180 mmol/day) and a high (380 mmol/day) dietary sodium intake. Plasma ANF and cGMP concentrations were less on the low than on the high sodium intake. Values for ANF on the medium sodium intake were intermediate. In normotensive subjects cGMP concentrations did not differ significantly on the low and the medium sodium intake. As compared with the controls plasma concentrations of cGMP were significantly increased in hypertensive patients on all three levels of sodium intake, while ANF concentrations were identical in the two groups. Since cGMP is a second messenger to ANF the data suggest an increased cellular response to ANF in patients with essential hypertension.     

Salt sensitivity in blacks. Salt intake and natriuretic substances

Accumulating evidence suggests that hypertension in blacks is manifested in part by impaired renal excretion of salt. Consequently, this study was performed to determine if hypertensive and normotensive black subjects differ in their ability to generate known natriuretic substances. Fourteen normotensive and 11 hypertensive blacks were maintained on constant metabolic diets containing either 40 or 180 mmol of salt per day for 14 days each. During the last 4 days of each salt intake period, urine was collected for measurement of sodium, dopamine, and norepinephrine. On the last day of each 14-day dietary period, blood pressures were measured, blood was collected for measurement of plasma atrial natriuretic factor (ANF) and aldosterone, and urine was collected over 2 hours for measurement of prostaglandin E2 (PGE2). Both the normotensive and the hypertensive groups manifested salt sensitivity; their mean arterial pressure rose by 7 +/- 0.2 and 6 +/- 0.2%, respectively, when salt intake was increased from 40 to 180 mmol/day. The hypertensive group exhibited decreased (p less than 0.05) dopamine excretion as compared with the normotensive group for both dietary salt intakes. Plasma ANF levels increased (p less than 0.05) in the hypertensive group, but not in the normotensive group, with increasing dietary salt. Plasma aldosterone and urinary norepinephrine and PGE2 were comparable in the two groups for both dietary salt intakes. These data suggest that salt sensitivity is not unique to hypertensive blacks but occurs in normotensive blacks as well. Decreased renal production of dopamine may be a pathogenic factor in the development and maintenance of hypertension in blacks.     

A randomized crossover study to compare the blood pressure response to sodium loading with and without chloride in patients with essential hypertension

Six patients with essential hypertension underwent a randomized cross over design study to investigate the effect of supplementing a 10 mmol/day sodium diet for a period of 5 days with either 120 mmol sodium chloride (Slow Sodium, Ciba, Horsham, UK) or 122 mmol sodium in the presence of other anions, mainly phosphate (Phosphate, Sandoz, Feltham, UK). With both sodium salts, urinary sodium excretion was increased. The calculated amount of sodium retained was similar for both the sodium chloride and sodium phosphate periods. However, with the addition of sodium chloride to the low-salt diet, there were increases in supine mean blood pressure whereas with the addition of sodium phosphate no change in mean blood pressure occurred. The supine mean blood pressure after supplementation with sodium chloride (119.8 +/- 4.3 mmHg) was significantly greater than that after sodium phosphate (113.3 +/- 4.5 mmHg), similarly, the standing mean blood pressure was greater after addition of sodium chloride than of sodium phosphate (122.3 +/- 4.20 versus 115.4 +/- 3.0 mmHg). With both salts there were similar but non-significant increases in weight and reductions in plasma renin activity (PRA) and plasma aldosterone (PA).     

Effect of beta-adrenergic receptor blockade on atrial natriuretic peptide in essential hypertension

Plasma levels of atrial natriuretic peptide (ANP) were measured in 32 untreated subjects with essential hypertension and in 31 patients undergoing long-term treatment with beta-blockers. Patients receiving beta-blockers had significantly higher mean plasma ANP levels (72.0 +/- 36.0 [SD] pg/ml) than did untreated hypertensive subjects (39.8 +/- 15.8 pg/ml; p less than 0.01) and healthy normotensive controls (33.9 +/- 16.6 pg/ml; n = 61, p less than 0.01), while the mean plasma ANP concentration in untreated hypertensive subjects was not statistically different from that in control subjects. Administration of atenolol, 50 mg/day, for 4 weeks to 10 untreated subjects resulted in a significant (p less than 0.001) rise in plasma ANP levels (from 38.8 +/- 9.5 to 68.7 +/- 20.6 pg/ml). In 31 patients undergoing long-term treatment with beta-blockers, multivariate regression analysis revealed that age, pretreatment mean blood pressure, and plasma concentration of cyclic 3',5'-guanosine monophosphate (cGMP) were significant predictors of plasma ANP levels. These results suggest that beta-adrenergic receptor blockade in patients with essential hypertension elevates plasma ANP levels with a concomitant rise in cGMP concentrations, and that increased ANP in plasma may play a role in the compensatory mechanism that operates in response to beta-adrenergic receptor blockade.     

Decrease in blood pressure and increase in total peripheral vascular resistance in supine resting subjects with normotension or essential hypertension

Hemodynamic changes in the supine resting position were investigated in 70 male subjects, consisting of 15 healthy volunteers with normotension (blood pressure of 113 +/- 7/70 +/- 5 mmHg, M +/- SD), 25 patients with borderline essential hypertension (143 +/- 12/90 +/- 6 mmHg) and 30 patients with established essential hypertension (166 +/- 13/108 +/- 6 mmHg). The supine position reduced blood pressure, heart rate, stroke volume and cardiac output (p less than 0.001), but increased total peripheral vascular resistance (p less than 0.001). The decrease in systolic blood pressure (p less than 0.01), stroke volume (p less than 0.05) and cardiac output (p less than 0.05), and the increase in total peripheral vascular resistance (p less than 0.01) were significantly greater in the borderline and established essential hypertensive groups than in the normotensive group. The results demonstrated that the decrease in blood pressure was due to a reduction in both heart rate and stroke volume, and that the decrease in stroke volume and increase in total peripheral vascular resistance seen in the supine position were greater in the hypertensive groups than in the normotensive group. These hyperresponses may contribute to the development and persistence of high blood pressure in patients with essential hypertension.     

Plasma prolactin, renin and catecholamines in young normotensive and borderline hypertensive subjects

It has been reported that patients with essential hypertension have high plasma prolactin levels and suggested that reduced central dopaminergic activity may be a factor in the pathogenesis of essential hypertension. This study examines the influence of posture on plasma prolactin, plasma catecholamines, plasma renin activity, blood pressure and heart rate in 24 patients with borderline hypertension (age 19 +/- 1 years) and 20 normotensive subjects matched for age and body mass index. Supine plasma prolactin levels were similar in both groups [borderline hypertension, 11.3 +/- 0.7 ng/ml; normotensive, 10.7 +/- 0.8 ng/ml (mean +/- s.e.m.)] and no increase in plasma prolactin was observed after 10 min standing in both groups. Normotensive and borderline hypertensive subjects had similar values for supine and upright plasma renin activity and plasma norepinephrine. There were no significant correlations between supine plasma prolactin and supine blood pressure, supine plasma renin activity or plasma norepinephrine when data from both normotensive and borderline hypertensive subjects were combined. These results may provide indirect evidence against the occurrence of reduced central dopaminergic activity in borderline hypertension.     

Walking 10,000 steps/day or more reduces blood pressure and sympathetic nerve activity in mild essential hypertension.

We investigated the effects of walking 10,000 steps/day or more on blood pressure and cardiac autonomic nerve activity in mild essential hypertensive patients. All subjects were males aged 47.0+/-1.0 (mean+/-SEM) years old. The original cohort consisted of 730 people in a manufacturing industry who measured the number of steps they walked each day using a pedometer. Eighty-three of these subjects walked 10,000 steps/day or more for 12 weeks. Thirty-two of these were hypertensives with systolic blood pressure (SBP) greater than 140 mmHg and/or diastolic blood pressure (DBP) greater than 90 mmHg. Thirty of these hypertensive subjects (HT) were examined twice, once during the pre- and once during the post-study period, for body mass index (BMI), maximal oxygen intake (Vo2max), blood pressure, heart rate (HR), and autonomic nerve activity by power spectral analysis of SBP and HR variability. In the HT group, walking 13,510+/-837 steps/day for 12 weeks lowered blood pressure (from 149.3+/-2.7/98.5+/-1.4 to 139.1+/-2.9/90.1+/-1.9 mmHg; p<0.01, respectively). In both the 34 normotensive controls and 17 hypertensive sedentary controls, blood pressure did not change. Walking also significantly lowered low-frequency fluctuations in SBP as an index of sympathetic nerve activity, from 1.324+/-0.192 to 0.738+/-0.154 mmHg2/Hz (p<0.05). VO2max rose significantly from 26.1+/-2.4 to 29.5+/-2.5 ml/kg/min (p<0.05). There were no changes in parasympathetic nerve activity, baroreceptor reflex sensitivity, or BMI. Our results indicate that walking 10,000 steps/days or more, irrespective of exercise intensity or duration, is effective in lowering blood pressure, increasing exercise capacity, and reducing sympathetic nerve activity in hypertensive patients.