(Hypertension. 1995;25:1301-1305.)
© 1995 American Heart Association, Inc.
Articles |
Twenty-Four–Hour Noninvasive Blood Pressure Monitoring and Pain Perception
From the Cattedra di Medicina Interna, II Facoltà di Medicina e Chirurgia, Università degli Studi di Pavia, Sede Varese, e Servizio di Fisica Sanitaria (L.B.), Ospedale Multizonale, Varese, Italy.
Correspondence to Dr Luigina Guasti, Divisione di Medicina Interna, Ospedale di Circolo, University Hospital, Viale Borri 57, 21100 Varese, Italy.
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Abstract |
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Abstract Although a hypertension-related hypalgesia has been described, the relation between pain perception and the 24-hour blood pressure trend is still unknown. The ambulatory blood pressure monitoring parameters and dental pain sensitivity were correlated in 67 male subjects. The pulpar test (graded increase of test current of 0 to 0.03 mA) was performed on three healthy teeth, and mean dental pain threshold (occurrence of pulp sensation) and pain tolerance (time when the subjects asked for the test to be stopped) were evaluated. Three groups of subjects with normal (n=34), intermediate (n=13), and high (n=20) blood pressure values were identified according to ambulatory monitoring results. Pain threshold differed among the three groups (P<.02), being higher in the group with highest blood pressure. The groups of hypertensive subjects showed higher pain tolerance than the normotensive group (P<.02). Pain threshold was correlated with 24-hour, diurnal, and nocturnal blood pressure values. Pain tolerance was also related to 24-hour blood pressure and to diurnal and nocturnal diastolic and mean arterial pressure values. Systolic and diastolic blood pressure loads were significantly associated with pain threshold, and diastolic load was also associated with tolerance. The blood pressure variability (SD) did not relate to pain perception. The 24-hour arterial pressure was more closely associated with pain perception than the blood pressure values obtained before the pulpar test. A close correlation between pain perception and 24-hour ambulatory blood pressure was demonstrated. The 24-hour mean blood pressure and loads, more than dynamic variations, were related to pain sensitivity, suggesting that the cardiovascular modulation of pain perception may be influenced mainly by sustained levels of arterial pressure.
Key Words: blood pressure • blood pressure monitoring, ambulatory • hypertension, essential • pain measurement • pain threshold
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Introduction |
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Hypertension-related hypalgesia has frequently been reported in animal studies and sometimes in humans.1 2 3 4 5 6 7 Electrical dental pulp stimulation (pulpar test) may be used to test the pain threshold because of its feasibility and safety.4 5 6 8 9 As the test current progressively increases, the pulpar test allows a quantification of the pain threshold. Tooth pulp contains only A-delta and C fibers, which are presumed to transmit only pain stimuli.10 11 Therefore, by testing the pain threshold with the pulpar test, it is possible to avoid interference from superficial sensations that could be triggered by other methods used to provoke pain. In recent years a strict relation between blood pressure (BP) values and endogenous opioids has become clear, demonstrating a secure role of the endorphins in the modulation of the cardiovascular system.2 12 13 14 15 16 17 18 Although conflicting results on the ß-endorphin plasma levels in hypertension were reported,7 19 20 an endorphin-related analgesia system seems to be associated with the finding of hypalgesia in hypertension.2 12 13 14 15
It is well known that BP values are greatly influenced by the emotional status of the patient and that casual measurements can be misleading.21 22 Twenty-four–hour ambulatory BP monitoring (ABPM) allows BP to be evaluated during daily life and gives more accurate data on hypertensive disease. Recently, this method has been used to point out some particular aspects of the day/night trend and to obtain information on the BP load and variability.21 23 24 25 26 27 28
The aims of this study were to correlate the 24-hour ABPM results with the dental pain threshold and tolerance in normotensive and hypertensive subjects and to assess the correlation between pain perception and dynamic pressure profile parameters such as BP load and variability.
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Methods |
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The study population consisted of 67 consecutive subjects referred to our center for ambulatory noninvasive BP monitoring, with the following characteristics: (1) no assumption of any therapy and/or pharmacological washout for at least 3 weeks before the monitoring; (2) male sex and age between 30 and 50 years; (3) a 5 mm Hg concordance between mercury column and pressure recorder readings on at least three consecutive measurements taken simultaneously on the same arm before the ABPM is begun; (4) a dental formula suitable for the pulpar test, as indicated by a previous dental checkup (subjects with tooth fractures, abrasions, caries lesions, fillings, and marked periodontal disease were excluded); (5) no concomitant diseases (diabetes, neuropathies, cardiac diseases, obesity, lung diseases, stroke, or psychiatric disturbances); (6) good-quality ABPM tracing (ie, valid measurements >80%); and (7) informed consent to the pain perception evaluation.
Fifteen of the 67 subjects were submitted to ABPM for a general clinical checkup, while 52 were sent from a general practitioner for BP evaluation. In all the subjects, routine diagnostic workup excluded secondary forms of hypertension. The average age of the subjects was 42±8 years.
Ambulatory BP Monitoring
Ambulatory BP was recorded by means of a noninvasive Takeda
TM2421 (A&D Co) set to take a measurement every 15 minutes for a period
of 24 hours. Measurement errors were minimized by the combined use of
the Riva-Rocci Korotkoff method and the oscillometric method for BP
measurements. If the auscultatory method did not permit a measure or
the parameters evaluated (BP and heart rate [HR]) fell into an
abnormal range (see below), the values obtained by the oscillometric
technique were shown in the integrated recording, after automatic
postprocessing. If the values obtained by the last method were also
abnormal, the measure was excluded automatically and shown as
"error." Measures were not considered valid when systolic BP
(SBP) was >280 or <60 mm Hg, diastolic BP (DBP) was >160 or <40
mm Hg, pulse pressure was >150 or <10 mm Hg, or HR was >200 or
<35 beats per minute.
In <15% of the measures of any single ABPM, the values were given according to the oscillometric technique. In 5 subjects in whom the quality of ABPM tracing was not sufficient (valid measures <80%), a second monitoring was performed successfully the following day.
The reading, editing, and analysis of data were provided by a computerized program (W. Pabisch spa) that gave the data as follows: (1) 24-hour SBP±SD, 24-hour DBP±SD, 24-hour mean BP (MBP), 24-hour HR±SD; (2) diurnal (6 AM to 10 PM) and nocturnal (10 PM to 6 AM) SBP±SD, DBP±SD, MBP, HR±SD29 ; and (3) percentage of measurements throughout 24 hours >140 mm Hg for the SBP (SBP load) and >90 mm Hg for DBP (DBP load). A mean 24-hour SBP <140 mm Hg and a mean 24-hour DBP <90 mm Hg were defined as normal.30
Pulpar Test
Dental pain perception evaluation was determined before
the ABPM by use of an electrical pulp stimulator commonly used in
dentistry for clinical purposes (MEDI-tester, MEDIC-AL).
Between 9 and 10 AM, the subjects were kept in a supine and comfortable position for 30 minutes, with the BP recorded every 3 minutes by an automatic Hewlett Packard 78352A recorder. Mean values of BP measurements obtained during the last 9 minutes were defined as baseline BP. Baseline BP and BP values obtained immediately before the pulpar test were evaluated in further statistical correlations. Afterward, the pulpar test was performed on three healthy teeth (two upper incisors and one inferior incisor, always in the same order). All the measurements were done blindly (ie, without the dentist's knowing the subject's BP).
The pulpar tester allows the delivery of automatic intermittent bursts of electrical stimuli with negative polarity at linearly increasing intensity from 0 to 0.03 mA (maximal tension, 6500 mV). The burst frequency was set to 5 Hz. The stimulator was applied to the tooth through a metal cylinder (ID, 0.9 mm) that was placed on the enamel surface with an electrode paste on the cylinder to improve contact. The circuit was closed by the hand of the operator placed in contact with the lips of the subject. Switching on and off occurred automatically when contact with the tooth was made or excluded, respectively. As the test current increased from 0 to 0.03 mA, a number from 0 to 80 (relative units, rU) was displayed on a digital reader of the instrument not visible to the subject under examination. The subjects were previously instructed to raise their right hand at the occurrence of pain or when they wanted to stop the delivery of the test current. Pain threshold (expressed in rU) was defined in all the subjects as the minimal intensity of test current that elicited any pulp sensation.9 At this point the stimulation was interrupted. The pain tolerance (rU) was obtained by reapplying the test current immediately afterward and keeping up the stimulation until subjects asked for the test to be stopped. The pain threshold and tolerance average values obtained by testing three teeth (as reported above) were used for subsequent analysis.
All the subjects were previously instructed to refrain from smoking and were asked not to take coffee, tea, chocolates, cola-containing drinks, and alcoholic beverages during the previous 12 hours. All the subjects gave their informed consent and were asked after any pulp stimulation whether they agreed to continue the study. All of them had a complete evaluation on three teeth.
The study was approved by the ethical committee of the hospital.
Statistical Analysis
Data are presented as mean±SD. Tests for homogeneity of
variances (Cochran's test and Bartlett-Box test) were performed. Since
the data obtained concerning pain perception were not homogeneous, they
were transformed into natural logarithms. Since the tests showed no
statistically significant differences among variances with respect to
the natural logarithm of both pain threshold and tolerance, one-way
ANOVA, the Scheffé test, the Student-Newman-Keuls test, contrast
method, and linear regression analysis were performed, with the
computerized SPSS (Statistical Package for the Social
Science) program. A value of P<.05 was considered
significant.
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Results |
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The subjects were divided into three groups according to the ABPM results. Group 1 consisted of 34 subjects with normal mean 24-hour BP. Group 2 consisted of 13 subjects with mean 24-hour SBP between 140 and 160 mm Hg and/or DBP between 90 and 95 mm Hg. Group 3 consisted of 20 patients with mean 24-hour SBP
160 mm Hg and/or mean 24-hour
DBP 95 mm Hg (Table 1).
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No difference was found between the groups with respect to age. The three groups differed significantly with regard to pain threshold (group 1, 3.11±0.23 ln rU; group 2, 3.28±0.28 ln rU; group 3, 3.33±0.34 ln rU; P<.02) and pain tolerance (group 1, 3.55±0.4 ln rU; group 2, 3.93±0.36 ln rU; group 3, 3.81±0.48 ln rU; P<.02) (Fig 1). The Scheffé test and the Student-Newman-Keuls test indicated the greatest difference in pain threshold between groups 1 and 3. The contrast method confirmed a significant difference among the three groups, with group 2 at an intermediate level. In regard to pain tolerance, Scheffé's test indicated a significant difference between group 2 and group 1, while the Student-Newman-Keuls test showed a difference between both group 2 and group 1 and group 3 and group 1. According to the contrast method, a difference was found between groups 2 and 3 and group 1.
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ABPM Parameters and Pain Perception
Pain perception was significantly related to mean 24-hour,
diurnal, and nocturnal BP values and with BP loads (Fig 2). The correlations between both pain threshold and
tolerance with ABPM parameters are shown in Table 2. The
SD of the 24-hour, diurnal, and nocturnal SBP and DBP were not related
to pain perception. The nocturnal BP fall (diurnal MBP - nocturnal
MBP, mm Hg, and coefficient of variation: diurnal MBP - nocturnal
MBP/diurnal MBPx100, %) was not associated with pain tolerance,
whereas a slightly significant negative correlation was found between
the coefficient of variation and pain threshold (r=-.21,
P<.05).
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Baseline BP Levels, Values Immediately Preceding the Pulpar Test,
and Pain Perception
Baseline BP values and those measured immediately before the
pulpar test by standard sphygmomanometry are shown in Table 3. When pain perception was correlated with baseline BP
and BP preceding the pulpar test, a significant correlation was found
between the diastolic and mean BPs and mean threshold (baseline
DBP/pain threshold: r=.32, P<.015; baseline
MBP/pain threshold: r=.26, P<.025; DBP before
pulpar test/pain threshold: r=.27, P<.025; MBP
before pulpar test/pain threshold: r=.26,
P<.025).
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Discussion |
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Since the first reports on hypalgesia occurring in animals with high BP values, various experimental data have provided clear evidence of the link between pain perception and BP levels.1 2 3 4 5 6 7 However, only a few authors have investigated this aspect of hypertension in humans, and all of them have correlated the experimental pain with casual arterial BP values measured in a clinical setting.4 5 6 7
This study was designed to associate dental pain perception with the 24-hour BP parameters obtained by means of a noninvasive ABPM.
Because of the great influence of environmental and emotional factors on BP levels, ambulatory monitoring is a better method than office measurements to provide a clearer and more accurate picture of the patient's status, especially in the case of borderline and mild hypertension.22 27 Moreover, it gives information on the 24-hour trend pattern of BP and on the BP load and variability.21 22 23 24 25 26 27 28 30 31 32 33
In this study, the dental pain threshold differed significantly among the three groups with normal, mildly elevated, and high BP values. Subjects with normal BP levels had the lowest pain threshold and hypertensive patients had the highest, whereas group 2 subjects were in between. Pain tolerance also was found to be different among the groups, being lower in normotensive subjects.
Electrical pulp stimulation is an ideal method to study pain threshold, and it has already been used in patients with hypertension and in patients with silent myocardial ischemia because of its characteristics.5 6 9 This test allows superficial sensations, such as pressure and touch, to be avoided. It stimulates fibers that are presumed to transmit painful sensation only and makes it possible to quantify the pain threshold and tolerance as the test current increases.9 10 11 Although the sensory aspect of conscious experience of pain involves the identification of painful sensation, the tolerance aspect is more variable and may depend on personality and situational and emotional factors.34
Pain sensitivity was significantly correlated with the mean values of the 24-hour, diurnal, and nocturnal systolic, diastolic, and mean BPs and with systolic and diastolic BP loads.
Conflicting results have been reported on pain perception and experimentally induced hypertension.35 36 37 A possible genetic substrate for hypalgesia in hypertension has been suggested by some authors.2 5 17 36 37 However, studies on experimental variations of BP seem to associate the pain-induced reflexes with the different BP levels.38 39 In our study, the correlation between pain perception and BP seems to indicate that different degrees of pain threshold are related to different BP levels.
In this study, the BP values measured both in baseline conditions and just before the pulpar test were significantly related to pain perception, confirming the finding of hypalgesia in hypertensive patients. However, a closer association was found between ABPM results and pain threshold and tolerance, suggesting the relevance of sustained BP levels in activating the cardiovascular mechanisms that may influence pain perception. Moreover, expectation related to pain evaluation on the day of the test may have influenced standard sphygmomanometric BP measurements.
The percentage of determinations that exceed the normal values has been used as an index of BP load.27 28 The role of sustained high BP on pain perception is also confirmed by the significant correlation between pain perception and BP load found with the present study.
On the other hand, fluctuations in BP do not seem to affect pain sensitivity. Although the 24-hour SD does not allow the separation of systematic BP variability (such as fluctuations between day and night), this parameter has been used as an index of BP variability.31 32 33 We did not find any correlation between the SDs and pain perception, even when the daytime and nighttime SDs were considered separately, as measures of low-frequency variability. This finding seems to indicate that the degree of BP variation does not consistently influence pain sensitivity. Also, pain threshold was negatively correlated with the nocturnal BP reduction, further suggesting that the persistence of elevated BP throughout the 24 hours is related to hypalgesia.
Various substances and various pathways are involved in pain transmission and pain modulation. At a central level, serotonin, substance P, catecholamines, and ß-endorphin (a potent endogenous opioidlike peptide) may act to influence painful sensations.40 The descending system of pain modulation extends from frontal cortex and hypothalamus, through the periaqueductal gray matter, to the rostral ventromedial medulla, and then to the dorsal horn.40 41 Activation of this system by opiates inhibits nociceptive dorsal horn neurons and produces analgesia.40 41 At the spinal level, the control of perception is affected by descending pathways, local actions of opiates, and local feedback.40 41 42 43 Circulating ß-endorphin may also be modulated by peripheral control through baroreceptor pathways.15 Also, the relevance to pain perception of vagal afferents has been described.2 15 18 44
In human studies, high circulating ß-endorphin levels have been suggested to explain both the absence of anginal pain and the generalized hyposensitivity related to silent myocardial ischemia.45 46 On the other hand, low pain thresholds and low endorphin levels have been described in patients with cephalea.47 Plasma catecholamines and substances such as cortisol do not seem to be related to pain perception in baseline conditions.48
It is controversial whether ß-endorphin plasma levels are higher in hypertensive than in normotensive subjects.7 19 20 However, since ß-endorphins are involved in pathways related to both cardiovascular control and pain modulation, a role of endogenous opiates as a link between hypertension and hypalgesia is very likely. This study suggests that dynamic variations of BP levels do not affect pain sensitivity, whereas stimuli from tonic and sustained BP elevation may influence pain perception. Moreover, pain sensitivity was related more to the 24-hour BP profile than to BP measured immediately before pain evaluation, suggesting that cardiovascular stimuli may influence the mechanisms underlying pain perception mainly through a long-lasting regulatory pattern.
Received April 15, 1994; first decision August 16, 1994; accepted January 18, 1995.
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References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Zamir N, Segal M. Hypertension-induced analgesia: changes in pain sensitivity in experimental hypertensive rats. Brain Res. 1979;160:170-173. [Medline] [Order article via Infotrieve]
2. Maixner W, Touw KB, Brody MJ, Gebhart GF, Long JP. Factors influencing the altered pain perception in the spontaneously hypertensive rat. Brain Res. 1982;237:137-145. [Medline] [Order article via Infotrieve]
3. Wendel OT, Bennett B. The occurrence of analgesia in an animal model of hypertension. Life Sci. 1981;29:515-521. [Medline] [Order article via Infotrieve]
4. Zamir N, Shuber E. Altered pain perception in hypertensive humans. Brain Res. 1980;201:471-474. [Medline] [Order article via Infotrieve]
5. Rosa C, Ghione S, Panattoni E, Mezzasalma L, Giuliano G. Comparison of pain perception in normotensives and borderline hypertensives by means of a tooth pulp-stimulation test. J Cardiovasc Pharmacol. 1986;8(suppl 5):S125-S127.
6.
Ghione S, Rosa C, Mezzasalma L, Panattoni E.
Arterial hypertension is associated with hypalgesia in
humans. Hypertension. 1988;12:491-497.
7. Sheps DS, Bragdon EE, Gray TF 3d, Ballenger M, Usedom JE, Maixner W. Relation between systemic hypertension and pain perception. Am J Cardiol. 1992;70:3F-5F. [Medline] [Order article via Infotrieve]
8. Andersson SA, Ericson T, Holmgren E, Linquist G. Electroacupuncture: effect on pain threshold measured with electrical stimulation of tooth. Brain Res. 1973;63:393-396. [Medline] [Order article via Infotrieve]
9. Falcone C, Sconocchia R, Guasti L, Codega S, Montemartini C, Specchia G. Dental pain threshold and angina pectoris in patients with coronary artery disease. J Am Coll Cardiol. 1988;12:348-352. [Abstract]
10. Azerad J, Woda A. Sensation evoked by bipolar intrapulpar stimulation in man. Pain. 1977;4:145-152. [Medline] [Order article via Infotrieve]
11. Kemppainen P, Pertovaara A, Huopaniemi T, Johansson G, Karonen SL. Modification of dental pain and cutaneous thermal sensitivity by physical exercise in man. Brain Res. 1985;360:33-40. [Medline] [Order article via Infotrieve]
12. Saavedra JM. Naloxone reversible decrease in pain sensitivity in young and adult spontaneously hypertensive rats. Brain Res. 1981;209:245-249. [Medline] [Order article via Infotrieve]
13. Feuerstein G. The opioid system and central cardiovascular control: analysis of controversies. Peptides. 1985;6(suppl 2):51-56.
14. Zamir N, Segal M, Simantov R. Opiate receptor binding in the brain of the hypertensive rat. Brain Res. 1981;213:217-222. [Medline] [Order article via Infotrieve]
15.
Brunner MJ, Wehberg KE, Williams JC, Cahill CA.
Carotid sinus baroreflex control of beta-endorphin release in
anesthetized dogs. Am J Physiol. 1989;256:R408-R412.
16.
Jin CB, Rockhold RW. Sympathoadrenal control by
paraventricular hypothalamic beta-endorphin in hypertension.
Hypertension. 1991;18:503-515.
17.
Farsang C, Kapocsi J, Juhasz I, Kunos G.
Possible involvement of an endogenous opioid in the
antihypertensive effect of clonidine in patients with essential
hypertension. Circulation. 1982;66:1268-1272.
18.
Sandor P, de Jong W, Wiegant V, de Wied D.
Central opioid mechanisms and cardiovascular control in
hemorrhagic hypotension. Am J Physiol. 1987;253:H507-H511.
19.
Farsang C, Vajda L, Kapocsi J, Malisak Z, Alfoldi S,
Varga K, Juhasz I, Kunos G. Diurnal rhythm of beta-endorphin in
normotensive and hypertensive patients: the effect of
clonidine. J Clin Endocrinol Metab. 1983;56:865-867.
20. Kraft K, Theobald R, Kolloch R, Stumpe KO. Normalization of blood pressure and plasma concentrations of beta-endorphin and leucine-enkefalin in patients with primary hypertension after treatment with clonidine. J Cardiovasc Pharmacol. 1987;10(suppl 12):S147-S151.
21. Pickering TG. Diurnal rhythms and other sources of blood pressure variability in normal and hypertensive subjects. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis and Management. New York, NY: Raven Press, Ltd; 1990:1397-1405.
22. Bottini PB, Carr AA, Prisant LM, Rhoades RB. Variability and similarity of manual office and automated blood pressures. J Clin Pharmacol. 1992;32:614-619. [Abstract]
23.
Verdecchia P, Schillaci G, Guerrieri M, Gatteschi C,
Benemio G, Boldrini F, Porcellati C. Circadian blood pressure
changes and left ventricular hypertrophy in essential
hypertension. Circulation. 1990;81:528-536.
24.
Pickering TG. The clinical significance of
diurnal blood pressure variations: dippers and nondippers.
Circulation. 1990;81:700-702.
25. Purcell HJ, Gibbs JS, Coats AJ, Fox KM. Ambulatory blood pressure monitoring and circadian variation of cardiovascular disease: clinical and research applications. Int J Cardiol. 1992;36:135-149. [Medline] [Order article via Infotrieve]
26. Wu MC. Analysis of blood pressure variability. Am J Hypertens. 1993;6:198S-200S. [Medline] [Order article via Infotrieve]
27. Zachariah PK, Sumner WE 3d. The clinical utility of blood pressure load in hypertension. Am J Hypertens. 1993;6:194S-197S. [Medline] [Order article via Infotrieve]
28. White WB, Dey HM, Schulman P. Assessment of the daily blood pressure load as a determinant of cardiac function in patients with mild to moderate hypertension. Am Heart J. 1989;118:782-795. [Medline] [Order article via Infotrieve]
29. The Scientific Committee: Consensus document on non-invasive ambulatory blood pressure monitoring. J Hypertens. 1990:8(suppl 6):135-140.
30. O'Brien E, Atkins N, O'Malley K. Defining normal ambulatory blood pressure. Am J Hypertens. 1993;6:201S-206S. [Medline] [Order article via Infotrieve]
31. Ruddy MC, Arora A, Malka ES, Bialy GB. Blood pressure variability and urinary electrolyte excretion in normotensive adults. Am J Hypertens. 1993;6:480-486. [Medline] [Order article via Infotrieve]
32. Devereux RB, James GD, Pickering TG. What is normal blood pressure? Comparison of ambulatory pressure level and variability in patients with normal or abnormal left ventricular geometry. Am J Hypertens. 1993;6:211S-215S. [Medline] [Order article via Infotrieve]
33.
Palatini P, Penzo M, Racioppa A, Zugno E, Guzzardi G,
Anaclerio M, Pessina AC. Clinical relevance of nighttime blood
pressure and of daytime blood pressure variability. Arch
Intern Med. 1992;152:1855-1860.
34. Fields HL. Neurophysiology of pain and pain modulation. Am J Med. 1984;77:2-8.
35. Zamir N, Simantov R, Segal M. Pain sensitivity and opioid activity in genetically and experimentally hypertensive rats. Brain Res. 1980;184:299-310. [Medline] [Order article via Infotrieve]
36.
Sitsen JM, de Jong W. Hypoalgesia in
genetically hypertensive rats (SHR) is absent in rats with experimental
hypertension. Hypertension. 1983;5:185-190.
37.
Feuerstein G, Zerbe RL, Faden AI. Opiate
receptors and cardiovascular control in conscious SHR and WKY
rats. Hypertension. 1983;5:663-671.
38. Maixner W. Interactions between cardiovascular and pain modulatory system: physiological and pathophysiological implications.J Cardiovasc Electrophysiol. 1991;2(suppl):S3-S12.
39. Randich A, Maixner W. The role of sinoaortic and cardiopulmonary baroreceptor reflex arcs in nociception and stress-induced analgesia. Ann N Y Acad Sci. 1986;467:385-401. [Medline] [Order article via Infotrieve]
40. Fields HL, Basbaum AI. Endogenous pain control mechanisms. In: Wall PD, Melzack Z, eds. Textbook of Pain. Edinburgh, UK: Churchill Livingstone; 1984:142-152.
41. Basbaum AI, Fields HL. Endogenous pain control mechanism: review and hypothesis. Ann Neurol. 1978;4:451-462. [Medline] [Order article via Infotrieve]
42. Yaksh TL. Spinal opiate analgesia: characteristics and principles of action. Pain. 1981;11:293-346. [Medline] [Order article via Infotrieve]
43.
Melzack R, Wall PD. Pain mechanism: a new
theory. Science. 1965;150:971-979.
44. Maixner W, Randich A. Role of the right vagal nerve trunk in antinociception. Brain Res. 1984;298:374-377. [Medline] [Order article via Infotrieve]
45. Sheps DS, Adams KF, Hinderliter A, Price C, Bissette J, Orlando G, Margolis B, Koch G. Endorphins are related to pain perception in coronary artery disease. Am J Cardiol. 1987;59:523-527. [Medline] [Order article via Infotrieve]
46. Falcone C, Specchia G, Rondanelli R, Guasti L, Corsico G, Codega S, Montemartini C. Correlation between beta-endorphin plasma levels and anginal symptoms in patients with coronary artery disease. J Am Coll Cardiol. 1988;11:719-723. [Abstract]
47. Genazzani AR, Petraglia F, Facchini V, Facchinetti F. Circulating beta-endorphin levels at various stages of life: possible connections with migraine pathogenesis. Cephalalgia. 1983;1:35-41.
48. Droste C, Meyer-Blankenburg H, Greenlee MW, Roskamm H. Effect of physical exercise on pain thresholds and plasma beta-endorphins in patients with silent and symptomatic myocardial ischemia. Eur Heart J. 1988;9(suppl N):25-33.
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