Sodium and Potassium Intake and Blood Pressure
GRAHAM
A.
MACGREGOR,
F.R.C.P.
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SUMMARY There is increasing circumstantial evidence that the very high sodium diet combined
with low potassium intake that most Western communities now eat may be, at least in part, responsible for the prevalence of high blood pressure. This circumstantial evidence combined with animal
evidence has been considered sufficient in some countries to make a general recommendation to
reduce sodium intake. If high sodium intake is an important cause of high blood pressure, it is not
clear at the present time how it may do so. In this report, evidence is reviewed for one hypothesis
suggesting an inherited defect in the kidney's ability to excrete sodium in patients who are going to
develop essential hypertension, together with evidence for a raised concentration of an inhibitor of
sodium transport. In patients with established hypertension, moderate restriction of sodium intake
appears to lower blood pressure and moderate potassium supplementation to also lower blood pressure. While further evidence is required, particularly long-term studies, it would seem prudent to
recommend to patients with essential hypertension or a strong family history of hypertension that they
restrict dietary sodium intake moderately and increase dietary potassium intake by the consumption
of more fruits and vegetables and, perhaps, the use of a potassium-based salt substitute. This regimen
could obviate or reduce the need for drug treatment in some patients with mild to moderate hypertension. (Hypertension 5 (supp III): III-79-III-84, 1983)
KEY WORDS • sodium intake • diet • potassium • kidney • heredity
transport inhibitor • epidemiology • natriuretic hormone
T
evolution and by individuals in communities today
where salt is not freely available.1"3 Concurrent with
this large increase in salt intake has been a smaller but
nevertheless potentially important reduction in potassium intake, partly from reduced consumption of fruits
and vegetables and partly from eating processed foods,
which have potassium removed during processing. It is
probable that potassium intake has fallen from 100 to
250 mmols/day previously to an average in most Westem communities today of between 30 to 80 mmols/
day. Does this high sodium/low potassium diet predispose us to the development of high blood pressure?
HERE is considerable controversy about the
role of sodium, first, as a cause of essential
hypertension and, second, whether its reduced intake has any effect on established high blood
pressure. Potassium intake may play a protective role
in preventing the development of essential hypertension and/or ameliorating it when it is established. From
an evolutionary point of view, sodium is a vital cation;
one of its major functions is to regulate the extracellular fluid volume. Over the centuries, because of the
obvious difficulties of obtaining sodium away from the
sea, mammals have developed powerful mechanisms
to conserve sodium in both urine and sweat and have
also developed an instinctual appetite to seek out sodium. We have acquired the ability to obtain salt both
from the sea and from mines and have found that it can
be used to preserve food during the winter. It re therefore not surprising that salt has become an extremely
important material, with great religious importance in
early civilizations and great economic significance. In
most developed countries, consumption of sodium is
extremely high, around 100-400 mmols/day compared
to the 5 to 10 mmols/day eaten by our ancestors during
Epidemiological Evidence of the Influence of
Salt and Potassium on Blood Pressure
There is considerable epidemiological evidence
from studying different communities that differences
in sodium and potassium intake among communities
are important determinators of the whole populations'
blood pressure levels. 12 - 4 All of these studies can be
criticized,5 but no study has produced evidence against
the concept. More recent studies in which potassium
excretion has also been measured suggest that within a
particular community there may be a direct relationship between potassium excretion or the sodium/potassium ratio in the urine and blood pressure. 6 ' 7 None of
these studies, however, is likely to demonstrate clearly
that altering sodium intake or potassium intake is going
From the Blood Pressure Unit, Department of Medicine, Charing
Cross Hospital Medical School, London, England.
Address forreprints:Dr. Graham A. MacGregor, Blood Pressure
Unit, Department of Medicine, Charing Cross Hospital Medical
School, London W6 8RF, England.
111-79
111-80
RESPONSE TO HYPERTENSION THERAPY
SUPP 111 HYPERTENSION VOL 5, No 5, SEPTEMBER-OCTOBER 1983
to affect blood pressure levels within that community.
Yet there are persuasive studies where communities
have changed their salt or potassium intake, such as the
Kenya study in which Samburu soldiers were given a
daily 16 g salt ration; a rise in blood pressure resulted,
part of which was ascribed to the increase in salt intake.8 An ongoing study of an African rural tribe, some
of whom have migrated to cities, has shown that blood
pressure is higher in urban environments and that perhaps at least part of the rise in blood pressure is related
to the increase in urinary sodium and fall in urinary
potassium that occurs in urban environments.9
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This abnormality in the kidney of the rat is most probably a difficulty in excreting sodium.13"13 In humans,
de Wardener and MacGregor 16 ' l7 suggested that those
who were going to develop essential hypertension
might have inherited a kidney that is less able to excrete sodium (fig. 1). The high sodium diet that we eat
in the West would give rise to a transient increase in
blood volume, triggering the release of natriuretic hormone that would inhibit sodium transport in the tubule
of the kidney, thereby increasing sodium excretion and
restoring sodium balance back toward normal. Blaustein18 has suggested that a raised level of a circulating
sodium transport inhibitor could increase intracellular
calcium concentration,18 by inhibiting sodium transport across the smooth muscle cell of the arteriole, and
thereby increase the sensitivity or tone of the arteriole.
Eventually, this would result in an increased peripheral
resistance and the development of high blood pressure.
The rate and severity of the hypertension would therefore depend on the extent of the kidney's defect in
excreting sodium and the amount of sodium in the diet.
An inhibitor of Na + -K + -ATPase has been demonstrated in normal human plasma, the level of which was
related to sodium intake." Two studies20'2I have shown
that the ability of plasma to inhibit Na + -K + -ATPase is
raised in patients with essential hypertension, as has
another study12 in which normotensive white cells incubated in hypertensive plasma acquired the same abnormality as the hypertensives' own white cells. The
protective effect of an increase in potassium intake on
sodium-induced hypertension could perhaps be explained apart from potassium's well-known natriuretic
effect, by potassium stimulating the sodium pump of
either the smooth muscle cell of the arteriole or the
A Possible Mechanism for Sodium Causing
High Blood Pressure?
The mechanism whereby a high sodium intake
might cause high blood pressure is not certain, but
most authors agree that there must be some defect in
the kidney's ability to excrete sodium. This could give
rise to retention of sodium and water, increased cardiac
output, and, by autoregulation, increased peripheral
resistance. However, the fact that plasma volume and
extracellular volume are not raised in essential hypertension, but tend to be reduced, makes this explanation
unlikely. On the whole, experimental evidence is
against this concept, and also does not explain the
increasing evidence of abnormalities of sodium transport in patients with essential hypertension.
In particular, there is evidence of inhibition of the
ouabain-sensitive component of the sodium pump.10"12
There is also evidence from kidney cross-transplantation experiments in animals that, in inherited hypertension in the rat, the kidney carries the underlying message for the later development of high blood pressure.
ORIGIN OF THE RISE IN ARTERIAL PRESSURE
IN INHERITED HYPERTENSION
+
N a intake
> 5O rnrnol
/day
ESSENTIAL
HYPERTENSION
ABNORMAL KIDNEY
"excretion f
r
Na excretion inadequate
? Dietary K
Total blood volume
normal (? transient rise)
or low
? Sympathetic
nerves
Intra thoracic
blood volume
Hypothalamus
\
Plasma N a + - K + ATPase inhibitor 4
? JG apparatus
? Adrenal
cortex
+
+
Na — K transport
SIDE
EFFECTS
FIGURE 1. Sequence of events to explain a postulated inherited defect in the kidney's ability to excrete sodium,
the observed rise in the concentration of a circulating sodium transport inhibitor, rise in salt intake, and the rise in
peripheral resistance in essential hypertension.
SODIUM AND POTASSIUM IKYAKE/MacGregor
sympathetic neuronal junction. Potassium is known to
oppose the effect of ouabain and could therefore oppose the raised levels of the circulating inhibitor of
Na + -K + -ATPase. In vitro, it is known that ouabain
increases norepinephrine output from nerve terminals
and reduces its reuptake, thus raising the amount of
norepinephrine available to react with receptor cells on
the affected cell membrane. It is possible, therefore,
that the increase in sympathetic activity that has been
reported in some patients with essential hypertension,
which also occurs with salt loading, could be due to an
increased concentration of the circulating sodium
transport inhibitor.
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Should the Whole Population Reduce Sodium
Intake or Increase Potassium Intake?
Recommendations in the U.S.A., Belgium, and,
more recently, the United Kingdom that the whole
population should reduce sodium and increase potassium intake are based not on direct experimental evidence but on animal and epidemiological evidence.
Many decisions by public health officials have to be
made before there is overwhelming scientific evidence. Previous public health measures such as vaccination for smallpox, provision of clean water, and
drainage at the time of the cholera and typhoid epidemics in Europe in the 19th century were taken under
similar circumstances.22 Indeed, the medical hierarchy
at the time opposed some of these changes, and evidence of their benefit only came retrospectively. If
communities are successful in altering the sodium/potassium ratio in their diet, careful observation of these
communities may provide the evidence to justify the
action that has already been taken. However, alteration
of sodium/potassium intake may only affect a small
proportion of the community, i.e., 10% to 20% of
those who already have or are going to develop high
blood pressure. Rose,23 however, has pointed out that
the benefits achieved by current blood pressure treatment would be equalled by a downward shift of the
whole blood pressure distribution of the population by
only a few mm Hg, since the risks from high blood
pressure increase throughout the range and do not start
at a particular diastolic or systolic pressure. However,
reducing sodium intake for a few days does not lower
blood pressure in normotensive subjects, largely because of an immediate compensatory rise in renin release,24 but a small study where potassium intake was
doubled by the use of slow potassium for 1 month did
show a small fall in blood pressure in normotensive
subjects.25
Established Hypertension
Once blood pressure is raised, removing the cause
does not necessarily lower the blood pressure level to
normal. Nevertheless, it has been known since the
early 1900s that severe restriction of sodium intake to
around 10 mmols/day does cause a substantial fall in
blood pressure in patients with severe and/or malignant
hypertension. In particular, the Kempner rice and fruit
diet,2* which was not only low in sodium but high in
111-81
potassium and low in protein, was an effective way of
lowering blood pressure but was extremely monotonous and most patients were not able to stick to it.
Studies in which sodium intake was increased from 10
mmols/day to around 25 to 35 mmols/day caused the
blood pressure to return toward treatment levels.27 It
was therefore assumed that less severe sodium restriction would not lower blood pressure and, with the
advent of diuretics, sodium restriction was abandoned
by many physicians. A more modest reduction of sodium intake, achieved by simply not adding salt to food
and avoiding high sodium foods has been claimed to
lower blood pressure in patients with mild to moderate
hypertension,28"30 but these studies have been criticized
for their lack of adequate controls, their open nature,
and the methodology of the blood pressure measurement.31
We therefore conducted a double-blind randomized
crossover study of the effect of modest restriction of
dietary sodium intake on unselected patients with mild
to moderate essential hypertension. We instructed 19
patients with mild to moderate essential hypertension
who had been under care of the Blood Pressure Unit for
some months to halve their sodium intake by not adding sodium to the food and avoiding sodium laden
foods. After 2 weeks of sodium restriction during
which their urinary sodium levels fell from 191 ± 19
mmols/24 hrs to 83 ± 11 mmols/24 hrs, they entered
into a double blind randomized crossover study of
Slow Sodium tablets for 1 month against identical
matching placebos for another month. The number of
Slow Sodium tablets that each patient took was estimated to restore sodium intake back to the subject's
usual intake. With sodium restriction, there was a significant fall in blood pressure; with placebo, the blood
pressure remained at the same level. With the increase
in salt intake with Slow Sodium, where urinary sodium
was restored back to their normal diet, blood pressure
rose. The percentage fall in blood pressure on the 4th
week of placebo compared to the 4th week of Slow
Sodium was 6.1%. 3 2
Our study, therefore, clearly demonstrated that
moderate restriction of sodium intake significantly
lowered blood pressure, and that its effect approximately equalled the effect of a single antihypertensive
drug such as a diuretic or beta-blocker (fig. 2).
Amery and coworkers28 demonstrated some time
ago that moderate sodium restriction is additive to diuretic therapy, and it is known that salt loading blunts
the blood pressure lowering effect of diuretics. A more
recent study has shown that moderate sodium restriction is additive to other drugs including betablockers.33 The immediate blood pressure lowering effect of sodium restriction, like a diuretic, is offset by
the rise in renin and angiotensin II that sodium loss
stimulates. Interfering with the release of renin or
blocking the formation of angiotensin II would therefore be expected to be especially effective in combination with sodium restriction. Use of drugs that block
the renin system, particularly the angiotensin converting-enzyme inhibitors, combined with moderate sodi-
111-82
RESPONSE TO HYPERTENSION THERAPY
NORMAL
WET
SUPP III HYPERTENSION VOL 5, No 5, SEPTEMBER-OCTOBER 1983
-SOOftJM RESTRICTIONSLOW
SODIUM
2nd 4th 2nd 4th
WEEK WEEK WEEK WEEK
PLACEBO
160
155
SYSTOLIC
PRESSURE 150
mm Hg
145
140
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100
DIASTOLJC
PRESSURE 95
mm Hg
90
150
URINARY
SODIUM 100
mmol/24 h
50
v
I
1
FIGURE 2. Average systolic and diastolic pressure and urinary sodium excretion in 19 patients with essential hypertension on a normal diet, 2 weeks after a restricted sodium diet,
and at 2-weekly intervals during the randomized crossover
study of Slow Sodium vs placebo. Patients were not receiving
any drug therapy. ***p < 0.001; **p < 0.07; *p < 0.05,
comparing equivalent measurements on Slow Sodium to placebo, tp < 0.001, comparing a normal diet to 2 weeks of dietary
sodium restriction.
drop in blood pressure. However, it has not as yet been
clearly demonstrated that potassium supplementation
is additive to the effect of sodium restriction. Nevertheless, based on the current evidence such as it is, it
would seem prudent to advise patients with essential
hypertension whether on treatment or not to restrict
sodium intake, or at the very least, not to add salt to
their food or to the cooking and to avoid sodium-laden
foods. An increase in potassium intake can be achieved
by the greater consumption of fresh fruit, vegetables,
and cereals, i.e., making the diet more natural. This
may carry other benefits apart from the increase in
potassium intake, particularly from the higher fiber
and lower saturated fat content of the diet. Use of a
potassium-based salt substitute may be helpful for
some patients following a low sodium diet and could at
the same time increase potassium intake.
All of these studies in patients demonstrate a blood
pressure drop in small groups of patients. The studies
have been criticized for the short length of time in
which the diets were altered. However, one study that
has been continued for a longer period of time showed
an increasing effect of moderate sodium restriction
with time,29 and it is certainly possible that moderate
sodium restriction might prevent the progressive rise
of blood pressure that can occur in patients with essential hypertension. Nevertheless, further studies of the
PREPLACEBO
FREATMENT 2nd week
4th week
160 -
~k
al
150 -
um restriction may therefore become more frequently
used in the treatment of mild to moderate hypertension.
There is considerably less evidence of the effect of
potassium supplementation in patients with essential
hypertension. One study in Japanese men34 who were
on a high sodium intake and studied as inpatients did
show a small decrease in blood pressure when potassium intake was doubled. We therefore conducted a
double-blind study of the effect of 8 Slow K (i.e., 64
mmols of potassium), which approximately doubled
potassium intake against placebo in a 1-month randomized crossover study of 23 patients with mild to
moderate essential hypertension who had been on no
treatment. This study,25 which had a run-in observation
period of at least 2 months, demonstrated that by approximately doubling potassium intake there was a
small but significant fall in systolic and diastolic blood
pressure (fig. 3).
A study by Holly et al.3* in which sodium intake was
reduced and potassium intake increased also showed a
SLOW POTASSIUM
2nd week 4th week
i
140 -
! ™ 100 -
°
<^
Si
|-§
*•
120
1
—L^
£:•:<
-
80
40
•X'!
•X*!
•X*'
i%
;X;
X**1
5S
X*I*
••V
xc
•X*
•X*!
t;X;
FIGURE 3. Average systolic and diastolic pressures and urinary potassium excretion before and during treatment with potassium and placebo. *p < 0.05; **p < 0.025; ***p < 0.001,
comparing equivalent measurement on Slow K to placebo.
SODIUM AND POTASSIUM IKTAKE/MacGregor
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effect of dietary alteration of sodium and potassium
intake in patients with essential hypertension must be
done and are much more easily done than lifelong
preventive community studies.
Future studies need to concentrate on whether increasing potassium intake is additive to the effect of
moderate sodium restriction and whether patients can
comply with the alteration of the diet over a long period of time, as well as which type of patient responds
best to dietary alteration. It is probable that the mechanism of the immediate fall in blood pressure with sodium restriction in patients with high blood pressure is
different from the mechanism by which sodium causes
a gradual rise in blood pressure over many years. Part
of the immediate fall in blood pressure with sodium
restriction is due to the lack of compensatory rise in
angiotensin II with sodium loss, and it is already
known that sodium restriction is more effective in low
renin patients. There is increasing evidence that drug
treatment of mild hypertension is beneficial. Approximately 10% to 20% of the population in the West have
a diastolic pressure over 90 mm Hg. The cost of blood
pressure lowering drugs could become extremely
large. Alteration of dietary sodium and potassium intake could play an important role in containing drug
costs in the future.
References
1. Denton D: The Hunger for Salt: An Anthropological, Physiological and Medical Analysis. Berlin, Heidelberg, New York:
Springer-Verlag, 1982
2. Gleibermann L: Blood pressure and dietary salt in human populations. Ecol Food Nutr 2: 143, 1973
3. Oliver WJ, Cohen EL, Neel JV: Blood pressure, sodium intake
and sodium related hormones in the Yanomamo indians, a
"no-salt" culture. Circulation 52: 146, 1975
4. Meneely GR, Battarbee HD: High sodium-low potassium environment and hypertension. Am J Cardiol 38: 768, 1976
5. Simpson FO: Salt and hypertension: a sceptical review of the
evidence. Clin Sci 57: 463s, 1979
6. Walker WG, Whelton PK, Saito H, Russell PR, Hermann J:
Relation between blood pressure and renin, renin substrate,
angiotensin II, aldosterone and urinary sodium and potassium
in 574 ambulatory subjects. Hypertension 1: 287, 1979
7. Khaw KT, Rose G: Population study of blood pressure and
associated factors in St. Lucia, West Indies. Int J Epidemiol.
In press
8. Shaper AG, Leonard PJ, Jones KW, Jones M: Environmental
effects on the body build, blood pressure and blood chemistry
of nomadic warriors serving in the army of Kenya. East Afr
Med J 46: 262, 1969
9. Poulter N, Khaw KT, Mugambe M, Peart WS, Rose G, Sever
P: Rural-urban migrant study of blood pressure and associated
factors in Kenya (abstr P3). British Hypertension Society
Meeting, Oxford, 1982
10. Moncam A, Borghi L, Canali M, Curti A, Perinotto P, Novarini A, Borghetti A: Altered sodium efflux in red blood cells
from essential hypertensive subjects. In Intracellular Electrolytes and Arterial Hypertension, edited by Zumkely H, Losse
H. New York: G. Thieme, 1980, pp 135-44
11. Edmondson RPS, Thomas RD, Hilton PJ, Patrick J, Jones NF:
Abnormal leucocyte composition and sodium transport in essential hypertension. Lancet 1: 1003, 1975
12. Poston L, Sewell RB, Wilkinson SP et al: Evidence for a
circulating sodium transport inhibitor in essential hypertension. Br Med J 282: 847, 1981
111-83
13. Dahl LK, Heine M: Primary role of renal homografts in setting
chronic blood pressure levels in rats. Circ Res 36: 692, 1975
14. Bianchi G, Fox U, Di Francesco GF, Giovanetti AM, Pagetti
D: Blood pressure changes produced by kidney cross transplantation between spontaneously hypertensive rats and norrnotensive rats. Clin Sci Mol Med 47: 435, 1974
15. Kawabe K, Watanebe TX, Shiono K, Sokabe H: Influence of
blood pressure on renal isografts between spontaneously hypertensive and normotensive rats utilizing the F| hybrids. Jpn
Heart J 20: 886, 1979
16. de Wardener HE, MacGregor GA: Dahl's hypothesis that a
saluretic substance may be responsible for a sustained rise in
arterial pressure. Its possible role in essential hypertension.
Kidney Int 18: 1, 1980
17. de Wardener HE, MacGregor GA: Natriuretic hormone and
essential hypertension. Lancet 1: 1450, 1982
18. Blaustein MP: Sodium ions, calcium ions, blood pressure regulation and hypertension: a reassessment and a hypothesis. Am
J Physiol 232 (suppl 3): C-I65, 1977
19. Chayen J: Effect of sodium intake on ability of human plasma
to inhibit renal Na + -K + -adenosine triphosphatase in vitro.
Lancet 1:411, 1981
20. MacGregor GA, Fenton S, Alaghband-Zadeh J, Markandu N,
Roulston JE, de Wardener HE: Evidence for a raised concentration of a circulating sodium transport inhibitor in essential
hypertension. Br Med J 283: 1355, 1981
21. Hamlyn JM, Ringel R, Schaeffer J, Levinson PD, Hamilton
BP, Avinoam Korwarski A, Blaustein MP: A circulating inhibitor of (Na + -K + )ATPase associated with essential hypertension. Nature 300: 650, 1982
22. Longmate N: King Cholera — The Biography of a Disease.
London: Hamish Hamilton, 1966
23. Rose G: Stragey of prevention: lessons from cardiovascular
disease. Br Med J 282: 1847, 1981
24. Parfrey PS, Markandu ND, Roulston JE, Jones BE, Jones JC,
MacGregor GA: Relation between arterial pressure, dietary
sodium intake, and renin system in essential hypertension. Br
MedJ 283: 94, 1981
25. Khaw KT, Thorn S: Randomised double-blind cross-over trial
of potassium on blood pressure in normal subjects. Lancet 2:
1127, 1982
26. Kampner W: Treatment of hypertensive vascular disease with
rice diet. Am J Med 4: 545, 1948
27. Watkin DM, Froeb HF, Hatch FT, Gutman AB: Effects of diet
in essential hypertension. II. Results with unmodified
Kempner rice diet in fifty hospitalized patients. Am J Med 9:
441, 1950
28. Parijs J, Joossens JV, Van der Linden L, Vergregen G, Amery
AKPC: Moderate sodium restriction and diuretics in the treatment of hypertension. Am Heart J 85: 22, 1973
29. Morgan T, Gillies A, Morgan G, Adam W, Wilson M, Carney
S: Hypertension treated by salt restriction. Lancet 1: 227,1978
30. Hunt JC: Management and treatment of essential hypertension.
In Hypertension, edited by Genest J, Koiw E, Kuchel O. New
York: McGraw-Hill, 1977, pp 1068-85
31. Swales JD: Dietary salt and hypertension. Lancet 1: 1177,
1980
32. MacGregor GA, Markandu ND, Best FE, Elder DM, Cam JM,
Sagnella GA, Squires M: Double-blind randomised crossover
trial of moderate sodium restriction in essential hypertension.
Lancet 1: 351, 1982
33. Beard TC, Cook HM, Gray WR, Barge R: Randomised controlled trial of a no-added-sodium diet for mild hypertension.
Lancet 2: 455, 1982
34. Iimura O, Kijima T, Kitchi K, Kikuchi K, Miyama A, Amdo
T, Nakao T, Takigami Y: Studies on the hypertensive effect of
high potassium intake in patients with essential hypertension.
Clin Sci 61: 77s, 1981
35. MacGregor GA, Smith SJ, Markandu ND, Banks RA, Sagnella GA: Moderate potassium supplementation in essential
hypertension. Lancet 2: 567, 1982
36. Holly JMP, Goodwin FJ, Evans SJW, Vandenburg MJ, Ledingham JM: Re-analysis of data in two Lancet papers on the
effect of dietary sodium and potassium on blood pressure.
Lancet 2: 1384, 1981
111-84
RESPONSE TO HYPERTENSION THERAPY
SUPP III HYPERTENSION VOL 5, No 5, SEPTEMBER-OCTOBER 1983
Discussion
DISCUSSANTS: A. SALVETTI
G. MACGREGOR
POOLE
G. WATT
What happens to normotensive subjects
being exposed to the same regimen?
SALVETTI:
Short-term sodium restriction in normals shows no fall in blood pressure because of
the reactive rise in renin and thereby angiotensin
II. We do not know the long-term effect of restricting sodium intake, particularly if you start at
an early age.
MACGREGOR:
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It is areallybig problem in our population
to restrict salt intake below 100 mg/day. So I
think that diuretic treatment is very important in
our population.
SALVETTI:
I think the most important point about Dr.
MacGregor's study is the initial level of blood
pressure of the patients studied, which was 98
mm Hg diastolic supine and 108 mm Hg diastolic
standing after 8 weeks of observation, giving an
average of 103 mm Hg. It is probable, therefore,
that the referral pressures were outside the mild
hypertension range. The mean level of blood
pressure during the 4th week of sodium restriction
was 96.5 mm Hg. I make three points; first, the
patients were not in the mild hypertension range;
second, pressure was not adequately controlled;
and third, if sodium restriction cannot control
pressure without additional drug therapy, it loses
much of its attraction for many patients.
WATT:
Before treating any patient, one must
exclude individuals who respond to placebo. In
your study, there was a large decrease in blood
pressure whether salt was restricted or not, and
your patients did not have mild hypertension. I
agree that our study was in patients with mild to
moderate hypertension, as we stated in the title of
MACGREGOR:
the paper. In this group of patients we demonstrated a significant fall in blood pressure with
moderate sodium restriction, roughly equivalent
to the effect of a diuretic.
POOLE: Could you tell us about the daily calcium
intake of your patients and comment on the work
of McKerron and colleagues as to whether calcium in an important dietary factor whose deficiency promotes hypertension and whose supplementation reduces blood pressure?
MACGREGOR: It is not appropriate to comment at present. We are doing studies on altering calcium
intake in normals and hypertensives and the effects of changing sodium balance on ionized calcium.
WATT: TOrespondto the comments that our patients
did not have mild hypertension, Dr. MacGregor
appears to be entertaining all possible explanations of our data other than the most reasonable
one, namely, that reducing sodium intake to less
than 60 mmol/day had no effect on blood pressure
in patients with pressures consistently in the range
90-99 mm Hg. We have good evidence to show
that the patients in our study correspond to roughly the 90th percentile of the blood pressure distribution in our population, which is mild hypertension in anybody's language.
MACGREGOR: During your study, the average diastolic pressure was 83 mm Hg. This is not mild
hypertension by anyone's definition. We have
now looked at your individual responses and because of the skewed nature of your randomized
crossover study, we applied nonparametric statistics arid found a significant effect of sodium restriction in your study.
Sodium and potassium intake and blood pressure.
G A MacGregor
Hypertension. 1983;5:III79
doi: 10.1161/01.HYP.5.5_Pt_2.III79
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