Clinical Science (2001) 100, 327–333 (Printed in Great Britain)
Comparison of nasal pH values in
black and white individuals with normal and
high blood pressure
N. J. IRESON, J. S. TAIT, G. A. MACGREGOR and E. H. BAKER
Department of Physiological Medicine, St George’s Hospital Medical School, Cranmer Terrace, London SW17 0RE, U.K.
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Salt-sensitive hypertension is common in people of African origin, and may be caused by
increased transepithelial sodium absorption. The pH of nasal secretions is negatively correlated
with the difference in Na+ concentration between nasal secretions and plasma, and may be a
marker of transepithelial sodium absorption. Nasal pH was measured using a probe sited under
the inferior turbinate. Measurements of nasal pH were reproducible, with a coefficient of
variation of 3.3 % for repeated measurements on the same day and of 2.7 % between measurements
on different days. Nasal pH did not correlate with nasal potential difference, a measure of
transepithelial sodium absorption. Nasal pH was significantly lower in 89 black individuals (24
normotensive and 65 hypertensive) than in 51 white individuals (26 normotensive and 25
hypertensive) (black normotensive. 6.44p0.08 ; black hypertensive, 6.62p0.05 ; white normotensive, 6.91p0.06 ; white hypertensive, 6.98p0.06), after adjustment for age, gender, current
smoking status, body mass index and 24 h urinary sodium excretion (P l 0.002), but was not
significantly different between the normotensive and hypertensive individuals. Nasal pH was
more acidic in black than in white individuals, which may represent generalized up-regulation of
sodium transport in black people. However, the lack of correlation between nasal pH and
potential difference suggests that nasal pH is, at best, only weakly related to transepithelial
sodium absorption. Ethnic differences in nasal pH may be of direct relevance in the airways, as
many of the functions of airway surface liquid are dependent on pH.
INTRODUCTION
Hypertension is common in people of African origin
living in urban societies. Nearly half of middle-aged
black U.K. residents and 76 % of African Americans
between the ages of 65 and 74 years have high blood
pressure requiring treatment [1,2]. Blood pressure is
generally more salt-sensitive in black people [3]. Black
people with hypertension have suppressed plasma renin
activity and angiotensin II levels [4], and excrete a sodium
load more slowly and less completely than white people
[5]. These features all suggest that a reduced ability of the
kidney to excrete sodium may underlie the development
of high blood pressure in black people.
Renal sodium transport cannot be measured directly,
as the renal tubule is not accessible to clinical assessment.
The airway epithelium shares many ion-transport proteins with the renal epithelium, is easily accessible in the
nose and may be useful as a model of renal sodium
transport. Measurements of trans-nasal potential difference have been used to demonstrate altered sodium
channel activity in Liddle’s syndrome, a monogenic form
Key words : African origin, blood pressure, Caucasian, nasal pH.
Abbreviations : BMI, body mass index.
Correspondence : Dr Emma Baker (e-mail ebaker!sghms.ac.uk).
# 2001 The Biochemical Society and the Medical Research Society
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of hypertension caused by activating mutations of the
epithelial sodium channel [6], and in pseudohypoaldosteronism type 1, a syndrome of low blood pressure
caused by inactivating mutations of the epithelial sodium
channel [7]. The pH of nasal secretions (nasal pH) may
also provide a measure of transepithelial sodium absorption. Nasal pH is usually acidic relative to plasma pH
[8,9]. In humans, nasal pH is negatively correlated with
the difference in Na+ concentration between nasal secretions and plasma, suggesting that H+ excretion could be
linked to Na+ absorption across the nasal epithelium [10].
This concept is supported by the finding that, in ferret
trachea, stimulation of secretion of airway surface liquid
using methacholine causes both an increase in the H+
concentration and a decrease in the Na+ concentration of
tracheal secretions, again suggesting a link between H+
excretion and Na+ absorption across airway epithelia
[11].
We hypothesize that increased transepithelial sodium
transport contributes to the development of high blood
pressure in black people. If nasal pH truly reflects
transpeithelial sodium transport, acidic nasal pH could
be used as a marker for increased transepithelial sodium
absorption. The aim of the present study was to investigate the relationship between nasal pH and sodium
absorption, as assessed by measurements of nasal potential difference, and to compare nasal pH between
black and white people with normal and high blood
pressure.
METHODS
Recruits
Validation of nasal pH measurement technique
Individuals were recruited from staff at St George’s
Hospital Medical School for repeat measurements of
nasal pH. Ethnicity and blood pressure were not recorded
in this group.
means of these three recordings. Hypertensive individuals had a systolic blood pressure of 140 mmHg and\or
a diastolic blood pressure of 90 mmHg. Normotensive individuals had a systolic blood pressure
of 140 mmHg and a diastolic blood pressure of
90 mmHg. Hypertensive individuals had not received
previous treatment, or had been off all drug treatment for
at least 2 weeks and diuretics for 4 weeks. People with
ischaemic heart disease, cerebrovascular disease, renal
impairment or other concurrent illness were excluded
from the study. Ethnicity was defined by skin colour,
place of birth or parents’ birth and cultural identity.
Where individuals were classified as ‘ black ’, African or
Caribbean ancestry was also noted.
In all studies of nasal pH measurement, individuals
were excluded from the study if they had any evidence of
acute or chronic rhinitis, asthma or atopy, or took nasal
drugs or any other drug that might interfere with
nasal epithelial function. Written informed consent was
obtained from all individuals prior to entry into the
study, which was approved by the Local Research Ethics
Committee of Merton, Sutton and Wandsworth. Procedures followed were in accordance with institutional
guidelines.
Clinical measurements
All individuals collected a 24 h urine sample 1–2 days
before attendance for nasal pH measurement, and this
was analysed for 24 h excretion of urinary sodium,
potassium and creatinine. On the day of nasal pH
measurement, individuals attended the Blood Pressure
Unit having had water, but no food or other beverages
from midnight onwards. Blood pressure, weight and
height were recorded. Smoking history was taken to
determine whether the subject had never smoked,
was an ex-smoker or was a current smoker. Serum
sodium, potassium, creatinine and urea were measured.
Plasma was analysed for plasma renin activity and plasma
aldosterone concentrations by RIA [13,14]. Individuals
then underwent measurement of nasal pH and nasal
potential difference.
Comparison of nasal pH in black and white individuals with
normal and high blood pressure
Measurement of nasal pH
Hypertensive individuals were taken from unselected
referrals by local general practitioners to the hypertension clinic. Normotensive controls were volunteers
from the local population recruited by advertisement, or
non-consanguineous relatives of hypertensive patients
attending the Blood Pressure Unit at St George’s Hospital. All individuals had their blood pressure measured
using an Omron HEM-705CP oscillometric blood pressure recorder [12]. Individuals rested for 5 min, after
which blood pressure recordings were done in triplicate
using the appropriate cuff size based on the upper midarm circumference. Blood pressure values given are the
Measurements of nasal pH were obtained using a portable
pH meter (Type 93-8052 ; Synectic Medical) and a
nasal pH probe (Type LoT440 ; Synectic Medical).
The nasal pH probe consisted of a single glass probe of
3 mm diameter, containing both reference and sensing
electrodes. Before measuring pH in each subject, the
probe was calibrated using buffered solutions of pH 7.01
and pH 1.01. The probe was sited under the inferior
turbinate of the right nostril. If the right nostril could not
be cannulated because of septal deviation, the left nostril
was used. pH was recorded at a depth of 4 cm from the
anterior nares until readings were stable for 10 s. All
# 2001 The Biochemical Society and the Medical Research Society
Ethnic differences in nasal pH values
readings were made by one of two operators. Operators
were not blinded to the ethnicity or blood pressure status
of individuals.
Validation of nasal pH measurement technique
To determine the repeatability and reliability of pH
measurements, individuals recruited for this part of the
study had nasal pH measured on two separate visits. On
the first visit, measurement of pH was carried out three
times in the same nostril, with the probe being washed in
distilled water between each recording. At a second visit,
at the same time on the next day, three measurements of
nasal pH were obtained in the same nostril using the same
protocol.
Comparison of nasal pH in black and white individuals with
normal and high blood pressure.
Black and white normotensive and hypertensive individuals each underwent one measurement of nasal pH
between 09.00 and 14.00 hours.
Measurement of nasal potential difference
Measurements of nasal potential difference were carried
out in black and white normotensive and hypertensive
individuals in the same nostril after measurement of nasal
pH was completed. Measurements were made by one of
two operators using the same set of equipment. Operators
were not blinded to the blood pressure status of the
individuals. Transmucosal nasal potential difference was
measured by a technique established previously in our
laboratory [15]. The reference electrode consisted of a
23 G butterfly needle, which was inserted into the subcutaneous tissue of the forearm. The exploring electrode
was an 8 G nasogastric tube filled with Ringer’s solution,
which was introduced along the inferior surface of the
inferior turbinate to a distance of 7 cm. Both electrodes
were connected to a high-impedance voltmeter by 1 %
Ringer’s agar bridges. The output of the voltmeter was
recorded continuously on a chart recorder throughout
the experiment. Nasal potential difference was recorded
from the inferior surface of the inferior turbinate as the
exploring electrode was withdrawn. The site of maximum
potential difference was established, and the measurement at this site was recorded once the voltage had been
stable for more than 5 s. A second measurement of the
maximum potential was made at the same site to ensure
consistency of recording, and the mean of these two
maximum values was taken as the potential difference for
analysis. Values were lumen-negative with respect to the
submucosa.
Statistical analysis
Group values are given as meanpS.E.M. for normally
distributed data, and as median and interquartile range
for plasma renin activity and aldosterone concentration,
which are not normally distributed. Two-way ANOVA
was used to compare nasal pH between black and white
individuals, and between normotensive and hypertensive individuals, before and after adjustment for age,
gender, body mass index (BMI), smoking status and 24 h
urinary sodium excretion. The difference in nasal pH
between ethnic groups was examined further using
Student’s paired t test to compare nasal pH between
subgroups of 15 black individuals and 15 white individuals (10 hypertensive and five normotensive in each
group) matched for age, gender, BMI and blood pressure.
Other differences between groups were tested using twosample t-tests for normally distributed variables and
chi-squared tests for categorical variables. Pearson correlation coefficients were calculated to examine relationships between nasal pH and nasal potential difference,
blood pressure and biochemical variables within black
and white normotensive and hypertensive groups. Twotailed P values of 0.05 were considered significant.
RESULTS
Validation of the nasal pH measurement
technique
To assess the repeatability and reliability of nasal pH
measurements, 20 individuals underwent three repeat
pH measurements on each of two consecutive days. The
average coefficient of variation for repeated measurements on the same day was 3.3 %, and that between days
was 2.7 %. These results suggest that pH measurements
are reasonably stable when recorded in an individual in
the same setting, and are consistent for the same person
on different days.
Comparison of nasal pH in black and white
normotensive and hypertensive individuals.
Groups of 24 black normotensive individuals, 65 black
hypertensive individuals, 26 white normotensive individuals and 25 white hypertensive individuals were studied.
The demographic characteristics of individuals are shown
in Table 1, and biochemical measurements are shown in
Table 2.
Nasal pH measurements
Nasal pH was more acidic in black than in white
individuals (black normotensive, 6.44p0.08 ; black hypertensive, 6.62p0.05 ; white normotensive, 6.91p0.06 ;
white hypertensive, 6.98p0.06) (Table 3). Two-way
ANOVA showed that nasal pH was significantly more
acidic in black than in white individuals (P 0.0001), but
was not significantly different between normotensive and
hypertensive individuals. The difference in pH between
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Table 1 Clinical characteristics of black and white individuals with normal and high blood
pressure
BP, blood pressure.
Black ethnicity
Variable
Normotensive
Number
Gender
Male :female
Female (%)
Age (years)
Males
Females
BMI (kg/m2)
Systolic BP (mmHg)
Diastolic BP (mmHg)
Smoking status (%)
Never
Ex
Current
Unknown
Table 2
White ethnicity
Hypertensive
Normotensive
Hypertensive
24
65
26
25
9 : 15
(62.5)
22 : 43
(66.2)
13 : 13
(50)
20 : 5
(20)
41.7p4.8
43.7p2.9
28.26p0.87
122.6p2.3
77.7p1.5
46.6p2.5
49.5p1.7
29.37p0.58
160.3p2.0
101.8p1.3
44.2p5.5
38.9p4.7
24.45p0.57
122.1p1.8
74.9p1.6
55.4p3.0
56.6p4.6
29.59p1.11
159.5p3.5
95.9p1.9
70.8
0
29.2
0
80
10.8
9.2
0
7.7
26.9
15.4
50
40
52
8
0
Biochemical characteristics of black and white individuals with normal and high blood pressure
Values are meanspS.E.M., except for plasma renin activity and aldosterone concentration, which are given as median (interquartile range).
Black ethnicity
White ethnicity
Variable
Normotensive
Hypertensive
Normotensive
Hypertensive
Plasma Na (mmol/l)
Plasma K (mmol/l)
Urine creatinine (mmol/24 h)
Urine Na (mmol/24 h)
Urine K (mmol/24 h)
Plasma renin activity (ng:ml−1:h−1)
Aldosterone (pmol/l)
138.8p0.29 (n l 22)
4.26p0.07 (n l 21)
13.4p0.8 (n l 19)
132.0p14.0 (n l 19)
56.3p3.4 (n l 19)
0.31 (0.12– 0.40) (n l 10)
317 (180–347) (n l 13)
139.4p0.23 (n l 63)
4.11p0.09 (n l 62)
13.7p0.6 (n l 57)
135.0p8.5 (n l 58)
64.2p2.7 (n l 58)
0.16 (0.1– 0.32) (n l 51)
342 (255–438) (n l 55)
139.7p0.4 (n l 18)
4.31p0.06 (n l 18)
11.1p0.6 (n l 11)
157.7p15.9 (n l 12)
77.5p4.3 (n l 12)
0.40 (0.30–0.92) (n l 8)
296 (172–478) (n l 11)
139.2p0.4 (n l 23)
4.28p0.08 (n l 23)
14.9p0.9 (n l 21)
140.8p8.6 (n l 23)
89.1p6.2 (n l 23)
0.51 (0.27–1.12) (n l 21)
450.5 (241–627) (n l 22)
Table 3 pH and calculated H+ concentration of nasal secretions in black and white
normotensive and hypertensive individuals
pH values are meanspS.E.M., and H+ concentrations are given as median (interquartile range).
Black
White
Variable
Normotensive
Hypertensive
Normotensive
Hypertensive
pH of nasal secretions
H+ concentration (nmol/l)
6.44p0.08
363 (302–437)
6.62p0.05
240 (214–269)
6.91p0.06
123 (107–141)
6.98p0.06
105 (91–120)
black and white individuals remained significant after
adjustment for age, BMI, gender and smoking status
(P l 0.002). The distribution of nasal pH values in black
and white individuals is shown in Figure 1. Further
analysis showed that nasal pH was not significantly
different between black people of African ancestry and
# 2001 The Biochemical Society and the Medical Research Society
black people of Caribbean ancestry [African, 6.63p0.06
(n l 28) ; Caribbean, 6.56p0.06 (n l 48) ; P l 0.43].
To confirm the relationship between nasal pH and
ethnic group, nasal pH measurements were compared
between subgroups of 15 black individuals and 15 white
individuals (10 hypertensive and five normotensive sub-
Ethnic differences in nasal pH values
Figure 1 Distribution of nasal pH values in black and white
individuals
Table 4 Clinical characteristics of 15 white individuals and
15 black individuals matched for age, gender, BMI and blood
pressure
Values are meanspS.E.M. BP, blood pressure.
Variable
African/Caribbean
(n l 15)
Caucasian
(n l 15)
Male : female
Age (years)
BMI (kg/m2)
Systolic BP (mmHg)
Diastolic BP (mmHg)
10 : 5
51.6p2.3
27.4p0.8
154.3p5.9
94.3p3.7
10 : 5
51.9p2.4
27.6p1.2
150.1p7.0
90.9p4.2
jects in each group) matched for age, gender, BMI and
blood pressure. Clinical characteristics of these matched
groups are shown in Table 4. Nasal pH was significantly
more acidic in the 15 black individuals than in the 15
white individuals (black, 6.59p0.11 ; white, 6.94p0.07 ;
P l 0.011).
Nasal pH and smoking status
Smoking status differed between the ethnic groups.
Significantly more white than black individuals were
current or ex-smokers (white, 68.4 % ; black, 22.5 % ; P
0.0001) (Table 1).
Observed differences in nasal pH between black and
white individuals were not accounted for by differences
in smoking status. Nasal pH was more acidic in black
than in white individuals when grouped by smoking
history (Figure 2). Nasal pH was significantly more
acidic in black than in white individuals after adjustment
for current smoking status, as well as for age, gender,
BMI and 24 h urinary sodium excretion (P l 0.002).
Relationship between nasal pH and other variables
Within each of the four groups of black and white
normotensive and hypertensive individuals, there was no
Figure 2 Nasal pH in black and white individuals with
different smoking histories
correlation between nasal pH and nasal potential difference, or between nasal pH and blood pressure, serum
biochemistry, 24 h urinary sodium or potassium excretion, or plasma hormone activity or concentration.
DISCUSSION
Our results show that nasal secretions are more acidic in
black people as a group than in white people. If nasal pH
truly is a surrogate measure of transepithelial sodium
absorption, then our findings suggest that sodium absorption is greater in black than in white people. In the
design of this study, we made two assumptions : that
nasal pH measurements could be used as a surrogate
marker for sodium absorption, and that nasal sodium
transport reflects renal sodium transport. In the interpretation of our results, it is first important to consider
the validity of these assumptions.
Nasal pH is usually acidic relative to plasma pH [8,9].
The maintenance of the pH of nasal secretions depends
on intact nasal epithelium ; nasal pH rises to more alkaline
values where the epithelium is damaged by infective or
allergic rhinitis [16]. The mechanisms by which nasal
secretions are made acidic, however, are not clear.
Nasal pH has been linked to sodium transport. In humans
the sodium gradient from nasal secretions to plasma is
negatively correlated with the pH of the nasal secretions.
This suggests that the greater the trans-nasal absorption
of sodium, the more acidic is the nasal pH [10]. In ferret
trachea, stimulation of the secretion of airway surface
liquid using methacholine causes both an increase in H+
concentration and a decrease in Na+ concentration of
tracheal secretions, again suggesting a link between
increased Na+ absorption across airway epithelium and
more acidic airway secretions. [11]. The predominant
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mechanism of sodium absorption across the airway
epithelium is through apical sodium channels. This
process generates a lumen-negative potential difference
that could drive the passive secretion of H+ ions, hence
linking increased sodium absorption with a fall in the pH
of airway secretions [17]. However, in the present study
we found no correlation between nasal pH and nasal
potential difference values in either ethnic group. These
observations suggest that sodium absorption through
epithelial sodium channels does not determine the pH of
nasal secretions. Other sodium transport processes described in airway epithelium, such as Na+\H+ exchangers
[18] and Na+–HCO − co-transporters [19], could also
$
link increased Na+ absorption with increasing acidity of
airway secretions. However, the contribution of these
transporters to overall sodium absorption is likely to be
small, and is unlikely to result in a good correlation
between sodium absorption and nasal pH. The assumption that nasal pH measurements reflect sodium absorption has not been explored further in the present
study, and requires future elucidation.
Nasal measurements of sodium transport can provide
some information about renal sodium transport. Where
sodium transporters are expressed in both the renal
tubule and the nasal epithelium, measurement of transporter activity in the nose could directly reflect activity of
that transporter in the kidney. For example, the epithelial
sodium channel is expressed in both the renal and nasal
epithelia [20,21]. Activating mutations of this channel in
Liddle’s syndrome result in increased renal tubular
sodium absorption and hypertension, which can also be
detected in the nose as increased nasal potential difference
[6]. Inactivating mutations of the epithelial sodium
channel in pseudohypoaldosteronism type 1 result in
decreased renal tubular sodium absorption with low
blood pressure, and can be detected in the nose as
decreased nasal potential difference [7]. Other sodium
transporters expressed both in renal [22] and airway [17]
epithelia include Na+\H+ exchangers, Na–K-ATPase
pumps and Na–K–2Cl co-transporters. It is probable
that structural abnormalities in these transporters would
also result in a change of transporter function in both
nasal and renal epithelia. The use of nasal measurements
as a surrogate for renal sodium transport does have
limitations. Although similar sodium transport proteins
are found in both the nose and the kidney, the transporters are regulated differently and hence may function
differently in the two tissues.
We have used nasal pH measurements to explore the
hypothesis that increased sodium absorption contributes
to the development of high blood pressure in black
people. Nasal pH did not correlate with nasal potential
difference, and therefore at best can be linked only
weakly to transepithelial sodium absorption. In the light
of this, few conclusions can be reached about the
pathogenesis of hypertension from the present study.
# 2001 The Biochemical Society and the Medical Research Society
Nasal pH was more acidic in black than in white subjects,
perhaps reflecting up-regulation of sodium absorption in
black people as a group. Although there was no difference
in nasal pH between hypertensive and normotensive
people within ethnic groups, and no correlation between
nasal pH and blood pressure, it is possible that most
black people have up-regulation of sodium transport, as
evinced by low nasal pH, but that the timing of the
development of hypertension depends on individual
exposure to precipitants such as high salt intake, low
potassium intake or other factors, such as obesity.
Our finding that black people as a group have more
acidic nasal secretions than white people may, however,
be of direct relevance in the airways. The pH of nasal
secretions is similar to the pH of surface liquid in the
lower airways [11,23], and many of the functions of
airway surface liquid are dependent on pH. For example,
acidic pH may confer an advantage in lung defence by
promoting the activity of lysozyme in airway surface
liquid [24] and inhibiting bacterial adhesion to airway
epithelial cells [25]. Conversely, the ability of antioxidants to scavenge free radicals (e.g. from ozone) is
impaired by an acidic pH [26]. The relevance of the pH of
airway secretions to the development of pulmonary
disease requires further elucidation.
ACKNOWLEDGMENTS
Measurements were made during a study funded by the
British Heart Foundation. We thank Nirmala Markandu,
Christine Carney, Rosemary Coulthard and Monique
Wood for recruitment of individuals and clinical
measurements, Alison Blackwood and Michelle Miller
for measurement of plasma renin activity and plasma
aldosterone concentration, Franco Cappuccio for assistance in identifying black normotensive individuals,
and Feng He for assistance with statistical analysis.
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Received 26 September 2000/30 October 2000; accepted 1 December 2000
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