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(Circulation. 2000;101:504.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
The Pressor Response to Water Drinking in Humans
A Sympathetic Reflex?
From the Clinical Research Center (J.J.), Franz Volhard Clinic, Berlin, Germany; Nathan Blaser Shy-Drager Research Program (J.J., J.R.S., B.K.B., Y.A., M.F., F.C., A.D., R.M.R., I.B., D.R.), Autonomic Dysfunction Center, and Department of Cardiology (B.K.B., R.M.R.), Vanderbilt University, Nashville, Tenn.
Correspondence to David Robertson, MD, Autonomic Dysfunction Center, AA3228 MCN, Vanderbilt University, Nashville, TN 37232-2195. E-mail david.robertson{at}mcmail.vanderbilt.edu
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Abstract |
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Background—Water drinking increases blood pressure profoundly in patients with autonomic failure and substantially in older control subjects. The mechanism that mediates this response is not known.
Methods and Results—We studied the effect of drinking tap water on seated blood pressure in 47 patients with severe autonomic failure (28 multiple system atrophy [MSA], 19 pure autonomic failure patients [PAF]). Eleven older controls and 8 young controls served as control group. We also studied the mechanisms that could increase blood pressure with water drinking. Systolic blood pressure increased profoundly with water drinking, reaching a maximum of 33±5 mm Hg in MSA and 37±7 in PAF mm Hg after 30 to 35 minutes. The pressor response was greater in patients with more retained sympathetic function and was almost completely abolished by trimethaphan infusion. Systolic blood pressure increased by 11±2.4 mm Hg in elderly but not in young controls. Plasma norepinephrine increased in both groups. Plasma renin activity, vasopressin, and blood volume did not change in any group.
Conclusions—Water drinking significantly and rapidly raises sympathetic activity. Indeed, it raises plasma norepinephrine as much as such classic sympathetic stimuli as caffeine and nicotine. This effect profoundly increases blood pressure in autonomic failure patients, and this effect can be exploited to improve symptoms due to orthostatic hypotension. Water drinking also acutely raises blood pressure in older normal subjects. The pressor effect of oral water is an important yet unrecognized confounding factor in clinical studies of pressor agents and antihypertensive medications.
Key Words: blood pressure • norepinephrine • water
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Introduction |
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The mechanisms that maintain water and electrolyte homeostasis in humans are relatively well-understood. Abnormalities in this balance and the physiological consequences of these abnormalities have been the focus of much research. Thus, fluid intake has often been viewed as just one of many regulatory factors in volume- and osmoregulation. Water ingestion increases blood pressure in several animal species.1 2 In humans, however, research on short-term cardiovascular effects of water drinking has been neglected, and the issue is not addressed in major physiology texts. The possibility that water drinking may have short-term cardiovascular effects came to our attention through observations made by patients with severe orthostatic hypotension due to autonomic failure. Several of these patients reported a substantial decrease in the severity of their orthostatic symptoms shortly after drinking water. We showed that drinking 480 mL water increased seated blood pressure 43 mm Hg in patients with autonomic failure and 11 mm Hg in older control subjects.3 This finding prompted us to further investigate the short-term effect of water drinking on blood pressure in patients with autonomic failure and in young and older normal controls. Furthermore, we endeavored to define the mechanism or mechanisms that could contribute to the pressor effect with water drinking.
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Methods |
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Subjects
We studied 47 patients with primary autonomic failure4 referred for disabling orthostatic hypotension. Twenty-eight patients (20 males, 8 females, 66±1 years) had multiple system atrophy (MSA, Shy-Drager syndrome), and 19 (8 males, 11 females, 72±2 years) had pure autonomic failure (PAF, Bradbury-Eggleston syndrome).4 Patients with secondary causes of autonomic failure (eg, diabetes mellitus, amyloidosis) were excluded. In addition, 11 older controls (7 males, 4 females, 57±2.2 years) and 8 younger controls (2 males, 6 females, 25±0.9 years) were recruited. Written informed consent was obtained before study entry. All studies were approved by the Vanderbilt institutional review board.
Protocol
Vasoactive medications and fludrocortisone were discontinued at
least 5 half-lives before testing. Studies were conducted at least 2.5
hours after breakfast or lunch. All blood samples were taken from an
antecubital heparin lock placed at least 30 minutes before sampling. In
patients, supine and upright blood pressure, heart rate, and plasma
catecholamines were determined. Patients and controls
underwent autonomic reflex testing that included determination of
respiratory sinus arrhythmia, a Valsalva maneuver, handgrip
testing, and cold pressor testing.5 In addition, we
conducted studies to determine the short-term
cardiovascular effects of oral or
intravenous water or oral yohimbine.
Oral and Intravenous Water Trials
In all patients and control subjects, the short-term effect of
water drinking on seated blood pressure was determined. Subjects were
seated in a chair with their feet on the floor. An automated brachial
blood pressure cuff (Dinamap, Critikon) was used. After 30 minutes of
baseline recording, subjects were given 480 mL tap water and
encouraged to drink it as quickly as possible. Seated blood pressure
and heart rate were recorded every 5 minutes for the next 90
minutes in patients, and for the next 60 minutes in control subjects.
In controls subjects, we obtained venous blood samples for the
determination of hematocrit, plasma catecholamines,
vasopressin, and plasma renin activity at baseline, and 30 and 60
minutes after water ingestion. In 4 patients, the pressor response to
drinking water at 2 different temperatures (9±0.5°C and 24±1.2°C)
was determined. In 4 patients, the blood pressure effects of drinking
480 mL and 240 mL on separate occasions were compared. In 5 patients,
the effect on blood pressure and plasma volume of drinking 480 mL tap
water was compared with the blood pressure effect an equal volume of
5% dextrose in water infused intravenously over a
60-minute period.
Oral Yohimbine Trial
Fifteen patients were tested on a separate day with 5.4 mg oral
yohimbine with 50 mL tap water; blood pressure was recorded in a
manner identical to the oral water trial. The pressor response to
yohimbine was compared with that of water.
Oral Water During Ganglionic Blockade
In 2 patients with autonomic failure due to multiple system
atrophy and in 7 younger control subjects, the pressor effect of water
after complete blockade of the autonomic ganglia was determined.
Subjects were studied while supine. In control subjects, an
arterial line was placed for continuous blood pressure
measurement. NN-cholinergic receptors were
blocked by continuous infusion of trimethaphan (Arfonad, Hoffmann
La-Roche) starting at a rate of 6 mg/min.6 7 We defined
complete blockade of the efferent arc of the baroreflex as <1 beat per
minute (bpm) change in heart rate with a 25 mm Hg increase or
decrease in systolic blood pressure obtained with bolus doses
of phenylephrine and nitroprusside,
respectively.7 When this end point was reached, the head
of the bed was raised slightly to allow for water drinking. The
subjects drank 480 mL tap water. The trimethaphan infusion was
continued at a constant rate during the period of
recording.
In the autonomic failure patients, trimethaphan was infused starting at a rate of 0.5 mg/min. The infusion rate was doubled every 6 minutes until no further change in blood pressure or heart rate occurred (maximum dose 8 mg/min). When this end point was achieved, the head of the bed was raised slightly, and the subjects drank 480 mL tap water while the trimethaphan infusion was continued at a constant rate.
Analytical Methods
Plasma catecholamines and plasma renin activity were
determined by standard methods.8 9 Plasma vasopressin
levels were determined by a radioimmunoassay. Hematocrit was determined
in quadruplicate using microcapillary tubes (International Equipment
Co, Model MB) centrifuged at 11 500 rpm for 10 minutes.
Relative plasma volume changes were determined on the basis of changes
in the hematocrit from the baseline value.10
Statistics
Results are presented as mean±SEM. Baseline
characteristics of subgroups were compared by unpaired 2-tailed
t test. Intraindividual comparisons were tested by paired
2-tailed t test. ANOVA was used for multiple comparisons.
Potential association between parameters was assessed by
linear regression analysis. The level of significance was set
at 
=0.05.
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Results |
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Autonomic Evaluation
Supine blood pressure was similar in MSA (157±5.2/85±3.4 mm Hg) and PAF (165±11/83±6; Table 1
). Supine blood pressure was lower in
younger (109±4.4/70±2.5 mm Hg) and older (122±4.8/79±3.5
mm Hg) patients than in autonomic failure patients (P<0.01
compared with MSA or PAF). Younger control subjects had lower supine
systolic blood pressure than older controls
(P<0.01); blood pressure decreased 70±4.7/28±2.6 in MSA
and 82±9.0/28±3.9 mm Hg in PAF mm Hg without an adequate
increase of heart rate while patients were standing. Patients with MSA
had higher plasma norepinephrine levels (2.2±0.57 nmol/L
[370±96 pg/mL]) than patients with PAF (0.88±0.29 nmol/L [150±49
pg/mL]; P<0.05). Plasma norepinephrine levels
increased when patients assumed the upright posture (3.4±1.2 nmol/L
[580±200 pg/mL] and 1.3±0.29 nmol/L [217±49 pg/mL] in patients
with MSA and PAF, respectively). Supine plasma renin activity was
relatively low in both patient groups (0.5±0.1 and 0.4±0.1 ng
· mL-1 · h-1 in
MSA and PAF, respectively) and did not significantly increase with
standing (0.56±0.13 and 0.67±0.21 ng ·
mL-1 · h-1 in MSA
and PAF, respectively).
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Sinus arrhythmia was markedly reduced in patients with autonomic failure. In both patient groups, blood pressure decreased profoundly during phase II of the Valsalva maneuver, and the blood pressure overshoot during phase IV was absent or blunted. Isometric exercise (handgrip test) and pain (cold pressor test) increased systolic blood pressure less in patients than in normal controls. In most patients, hyperventilation decreased systolic blood pressure. These responses are consistent with severe sympathetic and parasympathetic failure. In older controls, the sinus arrhythmia ratio (P<0.01) and Valsalva heart rate ratio (P<0.05) were significantly lower than in the younger control group.
Effects of Water Drinking on Blood Pressure
With water drinking, blood pressure increased 33±5/16±3
mm Hg in patients with MSA and 37±7/14±3 mm Hg in patients
with PAF (P<0.0001; Figure 1). The pressor response was evident
within 5 minutes after drinking started, reached a maximum after 
30
to 35 minutes, and was sustained for >60 minutes. Heart rate decreased
5±0.7 bpm in MSA and 2±0.8 bpm in PAF (P<0.001). The
pressor response after drinking either cold or warm water was almost
identical (Figure 2a). Drinking 480 mL
caused a greater pressor response than drinking 240 mL water (Figure 2b). Water drinking also increased systolic blood
pressure in healthy older controls, approaching a maximum of
11±2.4 mm Hg 35 minutes after drinking (P<0.001;
Figure 3). There was a concomitant
decrease in heart rate of 5.4±1.8 bpm below baseline 20 minutes after
drinking (P<0.001). There was no significant change in
blood pressure or heart rate in younger controls. Figure 4 illustrates individual changes in
systolic blood pressure in all groups during the 60 minutes
after water drinking. Data are expressed as area under the
curve.
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Effects of Water Drinking on Plasma Volume
In older controls, plasma volume changed by -0.1±0.9% and
-1.2±0.8% 30 and 60 minutes, respectively, after water drinking. In
younger controls, plasma volume changed by -1.0±0.9% and
-1.6±0.9% 30 and 60 minutes, respectively, after water drinking.
Similarly, there was no increase in plasma volume in 5 patients with
autonomic failure after water drinking (-0.2±0.7% after 30 minutes).
In the same patients, plasma volume increased by 5.3±2.0%
(P<0.05) after intravenous administration of
480 mL 5% dextrose in water. In these patients, oral water increased
systolic blood pressure 52±2.0 mm Hg, but
intravenous administration of 480 mL 5% dextrose in water
increased systolic blood pressure only 18±14 mm Hg.
Effects of Water Drinking on Plasma Catecholamines,
Renin, and Vasopressin
Thirty minutes after water drinking, plasma
norepinephrine increased in all 11 of the older control
subjects (by 0.61±0.29 nmol/L [103±49 pg/mL], P<0.05)
and in 6 of 7 younger controls (by 0.69±0.41 nmol/L [116±70 pg/mL],
P=0.14). In older and younger controls, plasma vasopressin
levels and plasma renin activity did not change significantly with
water drinking (Table 2). Similarly,
plasma vasopressin concentration did not change significantly in
autonomic failure patients (1.6±0.2 pg/mL at baseline, 1.6±0.2 pg/mL
30 minutes after drinking, n=6) after water drinking. Plasma renin
activity did not change after water drinking in 2 autonomic failure
patients who did have a pressor response.
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Effects of Water Versus Yohimbine on Blood Pressure
The 15 autonomic failure patients who were tested with both water
and yohimbine on separate days were stratified according to their
response to water (area under the curve) into 3 groups of 5 patients
each (small, intermediate, and large response). Patients with a greater
pressor response to water also had a greater pressor response to
yohimbine (P<0.01; Figure 5).
The response to yohimbine was quantified by calculating the area under
the curve of systolic blood pressure change between 30 and 90
minutes after the drug was given.
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Effects of Water During Ganglionic Blockade
In younger normal controls, the infusion rate of trimethaphan that
completely abolished baroreflex function was 6.6±0.3 mg/min. Blood
pressure decreased from 134±4.2/71±2.6 mm Hg at baseline to
98±3.1/54±2.6 mm Hg, and heart rate increased from 63±3.0 to
83±3.6 bpm with complete ganglionic blockade (P<0.0001).
Blood pressure did not change with water drinking during ganglionic
blockade. Plasma norepinephrine concentration decreased
from 1.3±0.12 nmol/L (220±21 pg/mL) at baseline to 0.31±0.03 nmol/L
(53±5.0 pg/mL) with complete ganglionic blockade (P<0.001)
and did not change with water drinking. The profound pressor response
to water drinking in 2 MSA patients was almost completely eliminated
with blockade of sympathetic and parasympathetic ganglia (Figure 6).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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These studies demonstrate that water drinking acutely elicits a profound pressor response in patients with autonomic failure. Water drinking also increases blood pressure in older normal control subjects, but it had no effect on blood pressure or heart rate in younger control subjects. Plasma volume, plasma renin activity, and plasma vasopressin concentration did not change with water drinking. If the pressor response to water drinking were mediated through an increase in plasma volume or release of a humoral factor, it should be augmented during complete ganglionic blockade. Ganglionic blockade, a condition which mimics complete autonomic failure,6 profoundly increases the sensitivity to pressor agents7 11 and to changes in cardiac preload.6 However, water drinking did not elicit a pressor response in younger controls during ganglionic blockade. Moreover, water drinking did not increase blood pressure in autonomic failure patients when residual autonomic transmission was blocked with trimethaphan.
The demonstration that the pressor response was not enhanced but rather
was abolished during interruption of ganglionic transmission indicates
that sympathetic or parasympathetic transmission are required.
Sympathetic activation is implicated by the observations that
-adrenoreceptor blockade with phentolamine
abolishes the pressor effect of water drinking in
animals,1 and that yohimbine (which acts through
sympathetic activation)8 12 had a greater pressor effect
in patients who displayed a pronounced pressor effect to water than it
did in patients with a moderate or absent pressor response to water.
Finally, in both younger and older controls plasma
norepinephrine levels increased after water drinking by a
magnitude at least as great as that elicited by smoking 2 unfiltered
cigarettes (97 pg/mL increase)13 or ingesting 250 mg
caffeine (102 pg/mL increase).14 15 The increase in plasma
norepinephrine concentrations could be due to sympathetic
activation causing increased spillover of
norepinephrine from adrenergic synapses into the systemic
circulation or to a decrease in norepinephrine
clearance.16 17 18
It seems paradoxical that a pressor response driven by sympathetic
activation could be exaggerated in patients with severe autonomic
failure, a condition that has previously been conceptualized as a
deficiency in autonomic function.19 20 In autonomic
failure patients, the loss of sympathetic and parasympathetic function
is less complete than that observed during complete ganglionic blockade
in normal subjects.6 Yohimbine, an 2-adrenergic
antagonist, increases sympathetic activity centrally and
augments norepinephrine release from postganglionic
adrenergic nerve endings.12 Yohimbine substantially
increases blood pressure in a large subgroup of autonomic failure
patients.12 21 22 It does not elicit a pressor response
during ganglionic blockade in normal controls.23 In
contrast, clonidine, an 2-adrenergic agonist, decreases blood
pressure in some autonomic failure patients and can increase blood
pressure in others.24 Therefore, the loss of sympathetic
function, even in patients with severe autonomic failure, is less
complete than is commonly believed.
Even though patients with autonomic failure may be able to release
norepinephrine, their capacity to do so is less than it is
in normal subjects.18 Thus, in autonomic failure, the
smaller amount of norepinephrine released causes a greater
increase in blood pressure. This phenomenon could be explained by
upregulation of vascular
1-adrenoreceptors25 26 or by impaired
baroreflex buffering.7 27 Impairment of baroreflex
function with aging28 might explain the observation that
water drinking increased blood pressure in normal older but not younger
controls. The afferent pathways that lead to sympathetic activation
with water drinking in humans are not known. In dogs, vagotomy
abolishes the pressor effect of moderate gastric distention with fluids
or a balloon.2 Possible factors that might trigger or
modulate the pressor response to drinking are distention of abdominal
viscera, as well as osmolarity and temperature of the fluids that are
given. When different fluids were infused into the stomachs of dogs,
distilled water was shown to cause a 2-fold greater increase in blood
pressure than normal saline.2 In humans, infusion of
hypoosmolar solutions through a gastric tube causes a greater increase
of sweat production, a sympathetic response, than infusion of
isoosmolar solutions.29 In our study, temperature did not
affect the pressor response to water.
Drinking water can provide a rapid relief of symptoms resulting from
orthostatic hypotension in autonomic failure patients. This
intervention is particularly useful in the morning (when
orthostatic hypotension tends to be more severe) and can
bridge the time required for oral medications to start working. In some
patients, water drinking increases systolic blood pressure by
>100 mm Hg, which can result in dangerously high blood pressure
in the supine position. In these patients, water drinking should
probably be avoided for 1.5 hours before retiring. Another important
implication of this study is that oral water intake needs to be
controlled in short-term pharmacological studies of pressor agents or
antihypertensive medications.
We conclude that drinking water rapidly raises sympathetic activity. In autonomic failure patients, this increase in sympathetic activity coupled with the incapacity to buffer any pressor stimulus profoundly increases blood pressure. It also substantially increases blood pressure in older but not detectably in younger controls. The pressor effect of oral water is an important, unrecognized confounding factor in clinical studies of pressor agents and antihypertensive medications. However, this effect can be exploited to improve symptoms resulting from orthostatic hypotension in patients with autonomic failure.
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Acknowledgments |
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This study was supported in part by NIH grants RR00095, P01 HL56693, and 1U01NS33460; NASA grant NAS 9-19483; and a grant from the Nathan Blaser Shy-Drager Research Program. Dr Jordan was supported by the Deutsche Forschungsgemeinschaft.
Received April 27, 1999; revision received September 9, 1999; accepted September 15, 1999.
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J E Naschitz, G Slobodin, N Elias, and I Rosner The patient with supine hypertension and orthostatic hypotension: a clinical dilemma. Postgrad. Med. J., April 1, 2006; 82(966): 246 - 253. [Abstract] [Full Text] [PDF]
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C. M. Brown, L. Barberini, A. G. Dulloo, and J.-P. Montani Cardiovascular responses to water drinking: does osmolality play a role? Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2005; 289(6): R1687 - R1692. [Abstract] [Full Text] [PDF]
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 Y.-I. Kamijo, T. Okumoto, Y. Takeno, K. Okazaki, M. Inaki, S. Masuki, and H. Nose Transient cutaneous vasodilatation and hypotension after drinking in dehydrated and exercising men J. Physiol., October 15, 2005; 568(2): 689 - 698. [Abstract] [Full Text] [PDF]
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R. E. Maser and M. J. Lenhard Cardiovascular Autonomic Neuropathy Due to Diabetes Mellitus: Clinical Manifestations, Consequences, and Treatment J. Clin. Endocrinol. Metab., October 1, 2005; 90(10): 5896 - 5903. [Abstract] [Full Text] [PDF]
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 A. Lipp, J. Tank, G. Franke, G. Arnold, F. C. Luft, and J. Jordan Osmosensitive mechanisms contribute to the water drinking-induced pressor response in humans Neurology, September 27, 2005; 65(6): 905 - 907. [Abstract] [Full Text] [PDF]
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C. Shibao, A. Gamboa, A. Diedrich, and I. Biaggioni Management of Hypertension in the Setting of Autonomic Failure: A Pathophysiological Approach Hypertension, April 1, 2005; 45(4): 469 - 476. [Abstract] [Full Text] [PDF]
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 T M Young and C J Mathias The effects of water ingestion on orthostatic hypotension in two groups of chronic autonomic failure: multiple system atrophy and pure autonomic failure J. Neurol. Neurosurg. Psychiatry, December 1, 2004; 75(12): 1737 - 1741. [Abstract] [Full Text] [PDF]
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J. Jordan, J. R. Shannon, A. Diedrich, B. Black, D. Robertson, and I. Biaggioni Water Potentiates the Pressor Effect of Ephedra Alkaloids Circulation, April 20, 2004; 109(15): 1823 - 1825. [Abstract] [Full Text] [PDF]
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M. Boschmann, J. Steiniger, U. Hille, J. Tank, F. Adams, A. M. Sharma, S. Klaus, F. C. Luft, and J. Jordan Water-Induced Thermogenesis J. Clin. Endocrinol. Metab., December 1, 2003; 88(12): 6015 - 6019. [Abstract] [Full Text] [PDF]
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C.-C. Lu, A. Diedrich, C.-S. Tung, S. Y. Paranjape, P. A. Harris, D. W. Byrne, J. Jordan, and D. Robertson Water Ingestion as Prophylaxis Against Syncope Circulation, November 25, 2003; 108(21): 2660 - 2665. [Abstract] [Full Text] [PDF]
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J. Tank, C. Schroeder, M. Stoffels, A. Diedrich, A. M. Sharma, F. C. Luft, and J. Jordan Pressor Effect of Water Drinking in Tetraplegic Patients May Be a Spinal Reflex Hypertension, June 1, 2003; 41(6): 1234 - 1239. [Abstract] [Full Text] [PDF]
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R. Corti, C. Binggeli, I. Sudano, L. Spieker, E. Hanseler, F. Ruschitzka, W. F. Chaplin, T. F. Luscher, and G. Noll Coffee Acutely Increases Sympathetic Nerve Activity and Blood Pressure Independently of Caffeine Content: Role of Habitual Versus Nonhabitual Drinking Circulation, December 3, 2002; 106(23): 2935 - 2940. [Abstract] [Full Text] [PDF]
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C. Schroeder, V. E. Bush, L. J. Norcliffe, F. C. Luft, J. Tank, J. Jordan, and R. Hainsworth Water Drinking Acutely Improves Orthostatic Tolerance in Healthy Subjects Circulation, November 26, 2002; 106(22): 2806 - 2811. [Abstract] [Full Text] [PDF]
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J. Jordan, A. Lipp, J. Tank, C. Schroder, M. Stoffels, G. Franke, A. Diedrich, G. Arnold, D. S. Goldstein, A. M. Sharma, et al. Catechol-O-Methyltransferase and Blood Pressure in Humans Circulation, July 23, 2002; 106(4): 460 - 465. [Abstract] [Full Text] [PDF]
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J. R. Shannon, J. Jordan, A. Diedrich, B. Pohar, B. K. Black, D. Robertson, and I. Biaggioni Sympathetically Mediated Hypertension in Autonomic Failure Circulation, June 13, 2000; 101(23): 2710 - 2715. [Abstract] [Full Text] [PDF]
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