The Sodium Intake Modifies the Renin-Aldosterone and Blood Pressure Changes Associated with Moderately Low Energy Diets

ABSTRACT. Thirty middle-aged, moderately obese men with untreated mild hypertension were allocated to two groups of 15 men each. Both groups were placed on energy-reduced diets (5.1 MJ/day) for 9–11 weeks which resulted in similar losses of body mass (8.5 kg). In group I the low energy diet was supplemented with sodium chloride leading to no change in urinary sodium excretion. During dieting there were significant reductions of plasma renin activity (PRA) and urinary excretion of noradrenaline and aldosterone. Heart rate but not mean arterial pressure (MAP) decreased significantly. Then followed a period of sodium restriction which resulted in a significant decrease in MAP and an increase in aldosterone excretion. In group II there was a reduction of sodium intake by about 80 mmol as judged from determinations of urinary sodium excretion. In this group the energy restriction was not accompanied by any changes in PRA or urinary excretion of aldosterone, whereas urinary noradrenaline excretion, heart rate and MAP decreased significantly. Urinary adrenaline excretion remained unchanged. It is concluded that the hypotensive response to moderate energy and sodium reduction cannot be explained by changes in the renin-aldosterone system.     

Effect of a Moderately Energy- and Salt-reduced Diet on Body Compartments and Blood Pressure Control in Obese Men with Mild Hypertension

Abstract Ten middle-aged moderately obese men with untreated mild hypertension were studied during a 6-week weight maintenance period and a 9-week period on a diet containing 5 MJ when body mass decreased by 8.4 kg (SE 1.4). According to urinary sodium excretion there was a mean reduction of 89 mmol/day (SE 16) in sodium intake. Mean arterial pressure fell by 2.5 to 14.1 mmHg (95% confidence interval) which was correlated to the reduction of body mass. The sympathetic nervous activity diminished with decreasing noradrenaline excretion and heart rate. There were no changes in the renin-aldosterone system. Estimation of the body composition with a four-compartment model utilizing determinations of body mass, total body potassium and total body water (TBW) showed reductions of body fat (8.4 kg (SE 1.4)) and body cell mass (BCM) (2.4 kg (SE 0.6)), but not of TBW. Extracellular water (ECW) increased significantly as judged from ECW/BCM calculations. Plasma volume was determined by Evan's blue and did not change significantly. We suggest that the observed changes in body composition represent one aspect of the adjustment to a weight reducing diet, while blood pressure is lowered by another mechanism in the adaptive response to dieting, i.e. reduction in sympathetic nervous activity.     

Reactivity to norepinephrine and effect of sodium on blood pressure during weight loss

Eighteen moderately obese middle-aged men with untreated mild hypertension were randomized to two groups and placed on a low energy diet regimen for 9 to 11 weeks. In Group I (n = 10) the amount of sodium chloride in the diet maintained the urinary sodium excretion at the predieting level. Mean body mass was reduced by 9.1 +/- 0.7 (SEM) kg. Mean intra-arterial pressure showed no significant change. There were significant decreases in heart rate (p less than 0.05) and urinary norepinephrine excretion (p less than 0.05) but not in plasma concentration of norepinephrine. In Group II (n = 8) energy as well as sodium intake was restricted, with a 95 +/- 22 mmol/24 hour reduction of urinary sodium excretion. Body mass decreased by 9.3 +/- 1.1 kg, and mean arterial pressure decreased by -18.9 to -4.3 mm Hg (95% confidence interval). There were also significant reductions in heart rate (p less than 0.001) and plasma norepinephrine concentrations (p less than 0.01) but not in urinary norepinephrine excretion. The pressor response (mean arterial pressure) to norepinephrine infusion at different dose rates was significantly elevated (p less than 0.05) in Group I during dieting in comparison with baseline. The blood pressure response to norepinephrine during dieting in patients in Group II was not changed from baseline.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sodium restriction and potassium supplementation in young people with mildly elevated blood pressure

Forty young subjects, aged 18 to 28 years, with mildly elevated blood pressure participated in a double-blind randomized three-period crossover study of the effect of sodium restriction with and without potassium supplementation on blood pressure. Dietary sodium intake was restricted for 18 weeks in which the patients received in random sequence 'slow-sodium' (90 mmol/day), 'slow-potassium' (72 mmol/day), and placebo tablets, each for 6 weeks. Mean urinary sodium excretion was 129 mmol/24 h in the slow-sodium period, 57 mmol/24 h during placebo, and 69 mmol/24 h during slow-potassium. Mean supine systolic blood pressure in the sixth week of the slow-potassium period was 3.3 mmHg lower than that at the end of the slow-sodium period (P less than 0.05). There was no significant difference in systolic or diastolic blood pressure between the placebo and the slow-sodium periods. The fall in systolic blood pressure in the low sodium/high potassium period was accompanied by a fall in cardiac index of 0.4 l/min per m2 body surface area (BSA) (P = 0.03). Our observations suggest a small hypotensive effect of moderate sodium restriction combined with high potassium intake in young hypertensive subjects. Sodium restriction alone has little effect on blood pressure in this group. The combination of a low sodium/high potassium diet may lower blood pressure by affecting cardiac output. Reducing the dietary sodium:potassium ratio may therefore be useful in the management of early primary hypertension.     

A study on the effects of a Mg-deficient diet on blood pressure and various hormonal systems in Wistar rats and spontaneously hypertensive rats

The influence of a Mg-deficient diet on blood pressure and various hormonal systems was examined in Wistar rats (WR) and spontaneously hypertensive rats (SHR). The WR and SHR were individually divided into 2 groups. The Mg-deficient diet was given to one group, and a Mg-containing diet was given to the other group for 3 weeks. During this experimental period, the body weight, blood pressure, urine volume, blood and urinary electrolytes, plasma steroid hormones, plasma renin activity (PRA), and urinary hormones [kinin, prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and noradrenaline] were examined. Although no significant difference in body weight was observed between the Mg-deficient and Mg-containing diet groups in either the WR or SHR (because the experiments were performed in a pair-fed fashion in both kinds of rat), the blood pressure was increased in the Mg-containing diet group but was unchanged in the Mg-deficient diet group. As regards changes in electrolytes, a decreased urinary excretion of Mg and significantly increased urinary excretion of P were observed in the Mg-deficient diet group in both the WR and SHR. Furthermore, decreased levels of serum Mg and P and increased levels of serum Ca were also noted. In the WR group, the urinary excretion of noradrenaline was significantly increased in the Mg-deficient diet group as compared to the Mg-containing diet group. However, the change was reversed in the SHR group. The plasma steroid hormones and PRA were both significantly low in the Mg-deficient diet group in both the WR and SHR. The urinary excretions of PGE2, 6-keto-PGF1 alpha, and kinin showed no significant differences between the two diet groups. The above results indicate that blood pressure is not affected by the Mg-deficient diet in either the WR or SHR, and the possible participation of the sympathetic nervous system in the mechanism of control of blood pressure may differ somewhat between the WR and SHR. In addition, Mg ion was found to play an important role in the biosynthesis of renin and steroid hormones but to have no such significant role in the urinary excretions of kinin, PGE2, and 6-keto-PGF1 alpha.     

The effect of modified fasting on blood pressure and sympathetic activity: a correlation?

The effect of a low calorie diet (200 kcal/0.8 MJ) composed of 50 per cent glucose and 50 per cent protein was studied on blood pressure and sympathetic activity in eight normotensive obese subjects. The study lasted 21 days; during the first seven days (period I) a weight maintaining diet was given; this was followed by 14 d (period II) of modified fasting (200 kcal/0.8 MJ). Sodium and potassium intakes of 20 and 80 mmol per d respectively were maintained constant throughout the study. In period I blood pressure decreased slightly until day 5; this occurred concomitantly with a marked natriuresis. Thereafter blood pressure and sodium excretion remained stable. No significant change was observed in the urinary excretion of total catecholamines, noradrenaline and 4-hydroxy-3-methoxy mandelic acid. From the start of period II blood pressure decreased markedly, together with a significant decrease in the urinary excretion of the catecholamines and 4-hydroxy-3-methoxy mandelic acid. Both blood pressure and urinary excretion of catecholamines and 4-hydroxy-3-methoxy mandelic acid stabilized after day 7 of period II. These changes preceded the maximal sodium diuresis of severe calorie restriction. The results suggest a primary role for the sympathetic system in the hypotensive effect of short term calorie deprivation although some influence of natriuresis cannot be excluded.     

Effect of Dietary Sodium Restriction on Patients Receiving Antihypertensive Medication

Twenty-four patients receiving medication for moderate to severe hypertension were studied during a six week normal diet and a six week low sodium period. Nean urinary sodium excretion was reduced from 169 ± 13 to 92± 7 mmol/24 hour yet with the exception of a small reduction in the mean erect systolic blood pressure 140.7 ± 2.5 to 135.1 + 2.6; p < 0.05) no significant alteration in the patients blood pressure was noted. Urinary potassium excretion and body weight remained unaltered. However, evaluation of the patient data when the patients were grouped into those taking thiazide diuretics (n = 14) and those not taking diuretics (n = 10) revealed a significant reduction in the mean supine systolic and diastolic and erect systolic blood pressure in the thiazide group. Significant changes in blood pressure were not recorded in the non-diuretic group. It is suggested that moderate dietary sodium restriction in combination with thiazide diuretics is of value in the treatment of moderate to severe hypertension     

Hypertension Produced by a High Sodium Diet in the Borderline Hypertensive Rat (BHR)

The effect of high dietary sodium (8%) on blood pressure in spontaneously hypertensive (SHR), borderline hypertensive (BHR), and normotensive Wistar-Kyoto (WKY) rats was determined weekly by tail cuff plethysmography for one week of baseline and four weeks of diet. After 4 weeks, significant elevations in systolic blood pressure were found in SHR and BHR groups, but not in WKY. BHR studied an additional 4 weeks showed a further progression of hypertension, reaching levels nearly equal to control SHR. Direct measurement of arterial pressure in conscious animals in their home cage confirmed the elevation in pressure in both SHR and BHR groups. Metabolic studies revealed that the high sodium diet reduced body weight in SHR and BHR strains, but not in WKY. Although both urinary volumes and sodium excretion values were significantly lower in SHR and BHR compared with WKY, this effect disappeared when adjustments for body weight were made.

Plasma norepinephrine determinations revealed a significant response to cold stress in all groups. Plasma epinephrine was elevated in all strains in response to cold stress; however, a consistent statistical elevation was seen only in WKY. The BHR is discussed as a model for determining the triggers responsible for environmentally-induced hypertension.     

Effect of energy-restricted diet on sympathetic muscle nerve activity in obese women.

Twenty obese women aged 45-65 years with borderline hypertension were allocated randomly to either a group with an energy-restricted diet or to a control group. Body weight, blood pressure, urinary sodium, and urinary excretion of norepinephrine and plasma volume were recorded. Resting muscle sympathetic nerve activity was measured in the peroneal nerve by tungsten microelectrodes and expressed as bursts per minute. These measurements were repeated after 3 days of semistarvation and after a body weight reduction of 7% while each patient's weight was in a steady state. After 3 days of semistarvation, only body weight was reduced, whereas after the long-term energy intake restriction, there were reductions of body weight (79.9 +/- 3.4 versus 74.1 +/- 3.4 kg; p less than 0.001), diastolic blood pressure (93 +/- 3 versus 86 +/- 4 mm Hg; p = 0.01), and muscle sympathetic nerve activity (49 +/- 2 versus 42 +/- 3 bursts/min; p less than 0.05). Other variables were unchanged. There were no changes in body weight, blood pressure, or muscle sympathetic nerve activity in the control group. We conclude that body weight decrease in obesity results in a reduction of blood pressure that is at least partially caused by a reduction of sympathetic vasoconstrictor activity.     

Effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and metabolic parameters in elderly normotensive individuals: a randomized double-blind crossover trial

OBJECTIVE: To examine the effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and parameters of glucose and lipid metabolism in elderly normotensive individuals. METHODS: We examined 21 healthy men and women aged 60-72 years in a randomized, placebo-controlled, double-blind crossover trial. After reducing dietary salt intake to below 100 mmol/day, study participants were randomly assigned to drink 1.5 l daily of a sodium chloride-rich (sodium 84.5 mmol/l, chloride 63.7 mmol/l, bicarbonate 21.9 mmol/l), a sodium bicarbonate-rich (sodium 39.3 mmol/l, chloride 6.5 mmol/l, bicarbonate 48.8 mmol/l) and a low-sodium (placebo: sodium, chloride and bicarbonate < 0.02 mmol/l) mineral water for 4 weeks each in a three-phase crossover order. Each phase was separated by a 2-week washout period in which the study participants remained on a low-salt diet. Compliance was assessed by biweekly urinary electrolyte excretion and five study participants were excluded from analysis for failing to complete the trial or to fulfil the compliance criteria. RESULTS: Mean arterial blood pressure was significantly lower during the periods of consuming low-sodium -7.0 +/- 7.2 mmHg, P < 0.001) or sodium bicarbonate-rich (-5.7 +/- 6.4 mmHg, P < 0.05) water than at baseline. In contrast, blood pressure during the phase of drinking sodium chloride-rich water was identical to that at baseline. Ambulatory 24 h blood pressure, oral glucose tolerance and plasma lipids were not affected by the different regimens. Urinary calcium excretion was significantly reduced by drinking low-sodium or sodium bicarbonate-rich water but was unchanged under the sodium chloride-rich water. CONCLUSION: Consumption of sodium chloride-rich mineral water can abolish the blood pressure reduction induced by dietary salt restriction in elderly individuals. Sodium bicarbonate-rich mineral water in conjunction with a low-salt diet may have a beneficial effect on calcium homeostasis.     

Dietary Sodium Intake and Urinary Dopamine and Sodium Excretion During the Course of Blood Pressure Development in Dahl Salt-Sensitive and Salt-Resistant Rats

ABSTRACT

Recent studies have suggested that dopamine (DA) formed within the kidney may play an important role in promoting sodium excretion, and that renal production and excretion of DA is determined by dietary sodium intake. Inasmuch as increased sodium consumption produces hypertension in Dahl salt-sensitive (DS) rats but not in Dahl salt-resistant (DR) rats, the present study was designed to examine the relationship between sodium consumption and urinary excretion of DA in these rats. DS and DR rats were placed on either high sodium chloride (8%) or low sodium chloride (0. 4%) diets at 4 weeks of age and their systolic blood pressure (SBP), urine volume, urinary sodium and catecholamine excretion were measured once every week for the next 4 weeks. High sodium chloride diet increased SBP in DS rats at 6 weeks of age and SBP continued to rise until they were 8 weeks old. The SBP of DR rats did not reach hypertensive levels when they were given high sodium chloride diet. The SBP of DS rats on low sodium chloride diet was significantly higher than DR rats on the same diet. The urinary DA excretion increased with age in all four groups of rats and was similar when they were 8 weeks old. However, both DS and DR rats on high sodium chloride diet excreted greater amounts of sodium and had increased urine volume compared to the DS and DR rats on low sodium chloride diet. There were no significant differences in urinary NE or E excretion in these four groups of rats. Kidney levels of DA and NE were significantly lower in DS compared to DR rats on high sodium chloride diet. These results show that although there are no differences in urinary DA excretion between rats on low and high sodium intake, both DS and DR rats on high sodium chloride diet are able to exhibit a natriuretic response. The DS rats eliminate sodium at the expense of an elevated SBP whereas DR rats stay normotensive. Therefore, it appears that alterations in mechanisms controlling renal vascular resistance rather than sodium excretion are responsible for the development of hypertension in DS rats.     

The Seasonal Variation of Blood Pressure in Patients with Essential Hypertension

We examined the role of dietary electrolytes and humoral factors in causing seasonal changes in blood pressure. Normal subjects had no seasonal difference in blood pressure, although urinary sodium and norepinephrine were significantly higher in winter than in summer. In patients with essential hypertension blood pressure, urinary sodium and norepinephrine excretion and plasma norepinephrine concentration were significantly higher in winter. Plasma renin activity, plasma and urinary aldosterone and urinary kallikrein excretion were not significantly different between the two seasons in both normal subjects and hypertensive patients. In conclusion, the blood pressure of patients with essential hypertension has a seasonal variation with higher pressures in the winter than in the summer.

Increased sympathetic nervous activity and an increased load of sodium presented to the kidney for excretion may be contributing factors in the rise in blood pressure in winter in patients with essential hypertension.     

Blood pressure response to hyperinsulinemia in salt-sensitive and salt-resistant rats.

We investigated the role of insulin in salt-sensitive hypertension in Dahl salt-sensitive and salt-resistant rats. The rats were kept in metabolic cages, and sodium intake and urinary sodium excretion were measured. In salt-sensitive rats receiving a 0.3% NaCl diet, sodium retention was significantly greater at weeks 1 and 2 in rats that received an insulin infusion than in those receiving a saline infusion. Mean arterial blood pressure and plasma norepinephrine levels were significantly higher at week 3 in insulin-treated rats than in saline-treated rats (mean arterial pressure, 137 +/- 3 mm Hg versus 119 +/- 3 mm Hg, p < 0.05; plasma norepinephrine, 0.40 +/- 0.02 ng/ml versus 0.27 +/- 0.01 ng/ml, p < 0.05). Insulin did not influence sodium retention, mean arterial pressure, or plasma norepinephrine in salt-resistant rats. Coadministration of an alpha-blocker (bunazosin, 10 mg/kg per day for 3 weeks) in salt-sensitive rats abolished the insulin-induced elevations in mean arterial pressure and sodium retention. When salt-sensitive rats were fed a low salt diet (0.03% NaCl), insulin did not raise mean arterial pressure. Thus, insulin elevated blood pressure only in the salt-sensitive model. The sympathetic nervous system and sodium retention in the early phase of insulin overload may contribute to elevation of mean arterial pressure in this model.     

DOMINANT EFFECT OF SUPPLEMENTED-SUCROSE ON THE LOW PROTEIN DIET-INDUCED INCREASE IN BLOOD PRESSURE OF SPRAGUE-DAWLEY RATS

A low-protein diet (LPD) is known to affect the regulation of hemodynamics, and could contribute to the genesis of hypertension. We investigated the mechanism for the LPD-induced elevation of blood pressure in 52 Sprague-Dawley rats. Rats fed the LPD for 8 weeks showed a significantly higher blood pressure than those fed on a normal-protein diet (NPD) when the LPD included sucrose as a predominant component of carbohydrate (LPD with a high sucrose content, 135 ±2 mmHg; NPD, 124 ±2 mmHg; p<0.05). However, LPD with a low sucrose content, in which corn starch was the main component of carbohydrate, did not have a hypertensive effect (125 ±2 mmHg). Urinary epinephrine and norepinephrine excretion was significantly higher in the LPD high-sucrose group than in the NPD and LPD low-sucrose groups, and there was a significant positive correlation between urinary norepinephrine excretion and systolic blood pressure. Urinary nitric oxide excretion was no different between these groups, and 2 % L-arginine administration exerted no antihypertensive effect on the LPD-induced elevation of blood pressure. Sodium restriction also did not attenuate the LPD-induced elevation of blood pressure. These results suggest that the effect of LPD on blood pressure could be interpreted as the effect of the high sucrose content supplemented to the LPD rather than the direct effect of protein restriction, and that the stimulation of sympathetic nervous activity was associated with this elevation of blood pressure.     

Dominant effect of supplemented-sucrose on the low protein diet-induced increase in blood pressure of Sprague-Dawley rats.

A low-protein diet (LPD) is known to affect the regulation of hemodynamics, and could contribute to the genesis of hypertension. We investigated the mechanism for the LPD-induced elevation of blood pressure in 52 Sprague-Dawley rats. Rats fed the LPD for 8 weeks showed a significantly higher blood pressure than those fed on a normal-protein diet (NPD) when the LPD included sucrose as a predominant component of carbohydrate (LPD with a high sucrose content, 135 +/- 2 mmHg; NPD, 124 +/- 2 mmHg; p<0.05). However, LPD with a low sucrose content, in which corn starch was the main component of carbohydrate, did not have a hypertensive effect (125 +/- 2 mmHg). Urinary epinephrine and norepinephrine excretion was significantly higher in the LPD high-sucrose group than in the NPD and LPD low-sucrose groups, and there was a significant positive correlation between urinary norepinephrine excretion and systolic blood pressure. Urinary nitric oxide excretion was no different between these groups, and 2 % L-arginine administration exerted no antihypertensive effect on the LPD-induced elevation of blood pressure. Sodium restriction also did not attenuate the LPD-induced elevation of blood pressure. These results suggest that the effect of LPD on blood pressure could be interpreted as the effect of the high sucrose content supplemented to the LPD rather than the direct effect of protein restriction, and that the stimulation of sympathetic nervous activity was associated with this elevation of blood pressure.     

Stress increases renal nerve activity and decreases sodium excretion in Dahl rats

The effects of a stressful environmental stimulus (air stress) on mean arterial pressure, renal sympathetic nerve activity, and renal function were examined in conscious Dahl salt-sensitive (DS) and Dahl salt-resistant rats (DR) on low (0.4%) and high (8%) NaCl diets. Air stress increased renal sympathetic nerve activity and decreased urine flow rate and urinary sodium excretion in conscious Dahl rats on a high sodium diet, but it had no effect in rats on a low sodium diet. Mean arterial pressure did not change during air stress in any group. Renal denervation prevented the antidiuretic and antinatriuretic responses to air stress in DS and DR on a high NaCl diet. An increased renal tubular reabsorption of sodium and water appeared to mediate the antinatriuretic and antidiuretic responses to air stress, since glomerular filtration rate and renal plasma flow were unchanged. Thus, environmental stress increases renal sympathetic nerve activity and decreases urinary sodium excretion more in Dahl rats on a high NaCl diet than on a low NaCl diet. On a high NaCl diet, these responses are greater in DS than in DR.     

Reduced sympathetic inhibition in salt-sensitive Japanese young adults

The purpose of our study was to investigate the sympathetic response to excess salt loading of 54 normotensive young adults with and without a family history of hypertension. We examined muscle sympathetic nerve activity, plasma concentration and urinary excretion of catecholamines, and ambulatory blood pressures during low (4 g NaCl) and high (16 g NaCl) salt diet intake. Ambulatory blood pressure and urinary excretion of catecholamines are known to be reduced during sleep. These parameters were therefore calculated during waking and sleeping periods. The subject was defined as salt-sensitive when mean ambulatory systolic pressure during the waking period was ≥3mm Hg higher during high salt intake than during low salt intake (n = 26: 21.4 ± 0.3 years old). When mean systolic pressure was either lower or equal during high salt intake than during low salt intake, the subject was defined as salt-resistant (n = 24: 21.3 ± 0.3 years old). Muscle sympathetic nerve activity, plasma concentration and urinary excretion of norepinephrine in salt-resistant subjects were significantly reduced (P < .05) by salt intake, wheras plasma concentration of epinephrine was unchanged and urinary excretion of epinephrine was reduced. In contrast, urinary excretion of epinephrine in salt-sensitive subjects was significantly elevated (P < .05) during high salt intake, whereas muscle sympathetic nerve activity and urinary excretion of norepinephrine remained unchanged despite a significant increase (P < .01) of ambulatory blood pressure. Of the salt-sensitive subjects, 73% (19 of 26) had a positive family history of hypertension, whereas only 5 of 24 salt-resistant subjects had a positive family history. These data indicate that the inhibition of sympathetic activity during a high salt intake did not occur in salt-sensitive young adults, and this may be linked with a hereditary predisposition to hypertension.     

Renal nerve contribution to NaCl-exacerbated hypertension in spontaneously hypertensive rats

Previous studies demonstrate that bilateral renal denervation enhances urinary sodium excretion and delays the onset of hypertension in young (7-week-old) spontaneously hypertensive rats (SHR) maintained on ordinary laboratory chow. We interpret these data as suggesting that increased renal nerve activity in this model contributes to hypertension by causing excess sodium retention. More recent studies show that dietary NaCl supplementation increases blood pressure and peripheral sympathetic nervous system activity in NaCl-sensitive SHR (SHR-S). The present study tests the hypothesis that the renal nerves contribute to the rise in arterial pressure caused by dietary NaCl supplementation in this model. SHR-S were fed a high (8%) or basal (1%) NaCl diet beginning at age 7 weeks. Bilateral renal denervation was carried out 2 weeks after the initiation of the diets, at which time systolic blood pressure was significantly higher in the high (compared with the basal) NaCl group. Systolic blood pressure was reduced slightly less in denervated SHR-S on the high (compared with basal) NaCl diet during the following 5 weeks. Renal denervation performed 1 week before initiation of the diets attenuated the subsequent development of hypertension equally in both groups. Both renal denervation and the high NaCl diet increased alpha 2-adrenergic receptor numbers in the kidney; renal denervation caused an approximately equal increase in alpha 2-adrenergic receptor binding in SHR-S on high and basal NaCl diets. The high NaCl diet increased plasma noradrenaline concentration, and renal denervation lowered mean arterial pressure but did not decrease circulating catecholamines in either diet group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Factors that Determine the Response of People with Mild Hypertension to A Reduced Sodium Intake

One hundred and eighty-six males who had had 3 run-in visits entered the study with a supine diastolic BP 95–110 mm Hg. This was followed by 3 pretreatment and 3 post-treatment visits. One hundred and sixty patients were given advice to reduce sodium intake after visit 3 and twenty-six patients served as control. In the control group there were relatively insignificant changes between the pre and post visits. In the diet group blood pressure fell by 13/9 mm Hg; urine sodium from 168 to 85 mmol/day and plasma renin activity rose from .50 to .77 ng AI/ml/h. Regression analysis showed that the only cross-sectional correlations were PRA with age, urine sodium and plasma potassium. There were highly significant correlations between the change in urinary sodium and the change in blood pressure and between the changes in blood pressure and plasma renin activity.

Multiple Regression Analysis indicated that the final diastolic blood pressure achieved depended upon the initial diastolic blood pressure, the fall in sodium intake, and was reduced by the rise in plasma renin activity. Patients who responded to sodium restriction had a lower initial renin value than other patients. This study emphasises the importance of the interaction between sodium, potassium and renin in the determination of blood pressure levels.     

Bartter's syndrome and diabetes mellitus

Abstract. We here report a case of Bartter's syndrome occurring in association with diabetes mellitus. The patient, an insulin-dependent diabetic, presented with hypokalaemia, inappropriate kaliuresis and metabolic alkalosis. He had high plasma renin activity, relatively low plasma aldosterone, and resistance to infused angiotensin II. A high potassium diet raised total body potassium and serum potassium, did not affect plasma renin activity, but raised plasma aldosterone significantly and did not alter the resistance to angiotensin II. Indomethacin administered acutely reduced urinary potassium and kallikrein excretion and, on chronic administration, lowered plasma renin activity, urinary chloride excretion, and raised serum potassium. Salt restriction resulted in a prompt and significant reduction in urinary sodium and chloride excretion. Urinary kallikrein excretion was very high throughout, increased with sodium restriction, and decreased with sodium loading. Oral potassium supplementation partially corrected the hypokalaemia, but did not affect blood sugar control. In this patient the primary defect appears to have been primary urinary potassium wasting, rather than sodium or chloride wasting. The striking effects of indomethacin suggest that prostaglandins may play a fundamental role in the genesis of the syndrome.