Clinical Science (1982) 63,4079-409s
407s
The effect of potassium and bicarbonate ions on the rise in
blood pressure caused by sodium chloride
T. 0. M O R G A N
Department of Veterans' Affairs and University of Melbourne Repatriation General Hospital, Heidelberg, Victoria, Australia
Summary
Methods
1. A group of eight patients with mild hypertension, sensitive to sodium intake, were studied.
2. Sodium chloride (70 mmol daily) caused
their blood pressure to rise by 19/14mmHg.
3. Sodium bicarbonate (70mmol daily) caused
their blood pressure to rise by 12/5mmHg.
4. Sodium chloride given together with
potassium chloride (70 mmol of each daily)
caused their blood pressure to rise by 9.6 mmHg.
5. These results suggest that sodium bicarbonate causes a smaller rise in blood pressure than
sodium chloride does and that potassium chloride
reduces the blood pressure raising effect of
sodium chloride.
6. A low sodium, high potassium and an
alkaline diet may therefore be a more effective
dietary method to reduce blood pressure than a
diet low in sodium alone.
The patients were eight males, age 55-70 years,
who were sodium sensitive in that they had a fall
in blood pressure of 10 mmHg or more when
their sodium intake was reduced. The patients
were maintained on this reduced sodium intake
throughout the study. After an equilibration
period of 2 weeks the patients were given a
placebo tablet for 2 weeks. They were then
randomly allocated to groups given either 70
mmol of NaCl or 70 mmol of NaHCO, daily for
2 weeks and were then crossed over to the other
treatment. All patients were then given 70 mmol
of NaCl together with 70 mmol of KCl daily for 2
weeks and finally were given placebo for 2 weeks.
On days 13 and 14 of each study period
patients were seen and blood pressures (phase I
and IV) were recorded in duplicate with an
amplified mercury sphygmomanometer after
lying for 10 min and again after 5 min standing.
Only the supine values are given here. Patients
were weighed and a 24 h urine collection was
made on each patient; this was analysed for Na+,
K+ and creatinine. Blood was taken for the
estimation of electrolytes, creatinine and plasma
renin activity.
The results in each study period were compared with those in the control period and with
each other by using a paired r-test, the values
obtained on day 13 and on day 14 of each study
period being used.
Key words: bicarbonate, potassium,
sodium.
renin,
Introduction
Most uncultured populations have a blood
pressure lower than Western populations and a
relative absence of vascular disease [ 1-31. Hypertension develops in these people when they move
into Western society and this has been attributed
to an increase in sodium intake. However, their
diet changes in many other ways, including a
reduction in potassium content and in alkalinity.
In this study we examined the influence of extra
potassium and bicarbonate on the hypertensive
effect of extra sodium.
Correspondence: Dr T. Morgan, Repatriation
General Hospital, Heidelberg West, 308 1, Victoria,
Australia.
Results
The patients in this study had all previously
reduced their sodium intake to half of their initial
intake. They had each had a fall in supine
diastolic blood pressure of 10 mmHg or more and
the average blood pressure in the group had fallen
from l6l/l05 mmHg to 142/89 mmHg. The
average values for weight, blood pressure and
408s
T. 0. Morgan
TABLE1. Weight,blood pressure, urinary electrolytes, serum K and plasma renin activity at the end of each period studied
Mean values are shown; n
Wt.
(kg)
=
8. Significance (paired t-test): P < 0.05 compared with first placebo value;
compared with NaCl value.
Supine blood pressure (mmHg)
Systolic
Pretreatment
Entry
Placebo
NaCl
NaHCO,
NaCl + KCI
Placebo
72.3.
69.7
69.6
70.6.
70.0.t
70.3.
69.6t
Serum K +
(mmolh)
Plasma renin activity
(pmol of ANG I h-I ml-')
Diastolic
161'
142
139
105.
158.
101.
147.t
148.t
1417
Urinary electrolytes
(mmol/day)
'!' P < 0.05
89
87
92'
93.
86t
urinary electrolytes did not differ significantly at
the entry point or during either placebo periods.
There was an increase of about 70 mmol/day in
urinary Na+ excretion in each study period and a
rise of about 70 mmol/day in urinary K+
excretion in the KCl supplemented period, suggesting that patients complied with the dietary
restriction and with the test procedures (Table 1).
Blood pressure rose by 19/14 mmHg (P <
0 4 0 1 ) when patients took 70 mmol of NaCl
extra each day. This blood pressure was similar to
the blood pressure measured 18 months earlier
before the patients were placed on a reduced
sodium intake. When NaHCO, was added to
their diet blood pressure rose by 12/5 mmHg
(P < 0.05) but this rise was significantly less than
that obtained with NaCl supplements. When KCl
was given as well as NaCl the blood pressure fell
by 10/8 mmHg ( P < 0.01) compared with that in
the NaCl period, but was higher than the value
obtained in the control period.
When NaCl was given weight rose in all
patients and there was a mean gain of 1 kg. When
NaHCO, was given the weight rose significantly
but the rise was less than that seen with NaCI.
The weight when the patients were on KCl as well
as NaCl was similar to the weight on NaCI.
Serum potassium fell when NaCl was added
and fell even further when NaHCO, was ingested.
Potassium chloride caused the serum K+ to rise
to a value similar to that of the controls.
There were no significant changes in sodium,
chloride, bicarbonate, urea or creatinine. Plasma
renin activity was reduced by sodium loading and
was reduced further by potassium loading (Table
1).
Discussion
The patients in this study were selected because a
reduction in sodium intake had caused a signi-
Na+
K+
204
95
84
157.
149.
156'
81t
39
41
44
46
51
113.t
46t
4.01
3.99
4.05
3.84.
3.5S.t
4.12"
4.06t
0.37.
0.48
0.50
0.25.
0.32.t
0.19t
0.46t
ficant fall in blood pressure [41. Sodium chloride
added to their diet increased blood pressure to a
value similar to that present before dietary
restriction of sodium. When the same amount of
sodium was given as sodium bicarbonate blood
pressure rose less than it did after sodium
chloride. Body weight rose after each supplement
but less after sodium bicarbonate. The distal
nephron is relatively impermeable to HCO: and
this means that less sodium is reabsorbed and its
excretion is aided. The greater fall in serum
potassium with sodium bicarbonate supports this
suggestion. Thus the increase in total body
sodium after sodium bicarbonate would be less
than after sodium chloride and the mechanism
leading to hypertension, whether this be humoral
[5-71 or volume [81 dependent. would be activated less.
Potassium chloride administration reduced the
rise in blood pressure due to sodium chloride and
this effect has also been observed in rats with
genetic hypertension [91. The mechanism is
unclear. It could be due to suppression of plasma
renin or a potassium chloride load, like the
bicarbonate load, may cause sodium to be
excreted more readily and thereby reduce body
sodium or volume so that the mechanisms leading
to hypertension are not activated. Alternatively
the potassium supplements may have specific
effects on 'cell transport of Na+ and K+, which
might ameliorate any effect on sodium transport
that is subsequent to sodium loading in people
with hypertension [51.
If these effects of sodium, potassium and
bicarbonate are shown to be separate and
additive then a more effective dietary treatment of
hypertension would be not only to reduce sodium
intake but also to increase potassium and bicarbonate intake. This could be achieved by eating
less processed foods and moving towards a more
vegetarian diet.
Potassium and bicarbonate ions and hypertension
Acknowledgments
This work was supported by the Life Insurance
Medical Research Fund of Australia and New
Zealand. The help of G. Morgan (R.N). is
acknowledged.
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