Psychosomatic Medicine
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Published online before print April 30, 2007, 10.1097/PSY.0b013e318050d6cc
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Holt-Lunstad, J.
Right arrow Articles by Steffen, P. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Holt-Lunstad, J.
Right arrow Articles by Steffen, P. R.
Related Collections
Right arrow Endocrinology
Right arrow Neuroendocrine
Right arrow Psychophysiology
Right arrow Sleep and Biological Rhythms
Right arrow Blood Pressure
Psychosomatic Medicine 69:339-343 (2007)
© 2007 American Psychosomatic Society

ORIGINAL ARTICLES

Diurnal Cortisol Variation is Associated With Nocturnal Blood Pressure Dipping

Julianne Holt-Lunstad, PhD and Patrick R. Steffen, PhD

From the Department of Psychology, Brigham Young University, Provo, Utah.

Address correspondence and reprint requests to Julianne Holt-Lunstad, Department of Psychology, Brigham Young University, Provo, UT 84602-5543. E-mail: julianne_holt-lunstad{at}byu.edu


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Objective: To investigate if diurnal cortisol variation is associated with nocturnal blood pressure (BP) dipping.

Methods: In this study, 302 healthy adults (51% female; average age 31 years) underwent 24-hour ambulatory BP assessment with BP measured randomly approximately every 20 minutes during waking hours and every hour during sleep. Salivary cortisol was obtained at five time points. Cortisol and BP have natural diurnal variations and disruptions in these diurnal variations are related to pathological conditions, such as greater risk for cardiovascular disease. A lack of a drop in cortisol from day to night and a lack of a drop in BP from waking to sleeping have both been associated with negative outcomes. It is not known, however, if diurnal variations in cortisol and BP are related, or if changes in cortisol from day to night influence BP dipping.

Results: Diurnal cortisol variation was a significant predictor of BP dipping. Controlling for gender, body mass index, age, phase of menstrual cycle, sleep quality, morning cortisol, and daytime measures of the relevant cardiovascular assessments did not significantly affect the results. Cortisol variation was found to have a stronger relationship with BP dipping than any of the covariates measured.

Conclusion: Decreased diurnal variation in cortisol is associated with decreased diurnal variation in BP. Future studies could benefit from examining how these two variables interact in predicting disease outcomes.

Key Words: ambulatory blood pressure • cortisol • circadian rhythm • cardiovascular functioning • health

Abbreviations: BP = blood pressure; SBP = systolic blood pressure; DBP = diastolic blood pressure; SES = socioeconomic status; HPA = hypothalamic-pituitary adrenalcortical; BMI = body mass index; AUC = area under the curve.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHOD
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Both cortisol and blood pressure (BP) have well-documented circadian rhythms and psychosocial factors, such as stress, have been shown to disrupt normal diurnal variation. Normally, cortisol levels peak in the early morning and drop to the lowest concentration at night (1–3). One way in which stress may affect the endocrine response is via disrupted circadian rhythms. The result can be manifest in higher evening cortisol levels or "flattened" curves (4,5). Evidence of this can be seen in disruptions in diurnal rhythms of cortisol among people exposed to chronic stress (6–9).

The BP circadian rhythm is typically characterized by minor fluctuations throughout the day and night, with an overall decrease (or dipping) that occurs during the night. Normotensive patients with mild-to-moderate hypertension typically show a 15% to 20% reduction in BP during sleep. However, a lack of nocturnal BP dipping may occur and is more prevalent among those with various disease states (e.g., hypertension, sodium sensitivity, chronic renal failure, sleep apnea, Cushing’s syndrome, and autonomic nervous system dysfunction) (10). Although disrupted BP rhythms have primarily been examined among nonnormal samples, a lack of dipping also occurs among normal individuals and factors, such as stress and socioeconomic status (SES), have been implicated in the cause. Research has demonstrated that chronically stressed individuals also show altered BP rhythms (11,12).

Importantly, disruptions in normal patterns of cortisol and BP have both been linked to negative health outcomes. For instance, the effect of cortisol disruption has been linked to immunosuppression, metabolic problems, Addison’s disease, Cushing’s disease, and even increased mortality. For example, flattened cortisol slope (lack of normal diurnal variation) predicted earlier mortality 7 years later among patients with metastatic breast cancer (13). A lack in BP dipping has also been associated with increased health risks including left ventricular hypertrophy (14,15), kidney damage (16), cerebrovascular stroke (17), cardiovascular morbidity (18), and even increased mortality (19,20). Thus, a disrupted circadian rhythm may have important long-term health implications.

Although a large research literature examines hypothalamic-pituitary adrenalcortical (HPA) and sympathetic function, it is not well understood the extent to which these distinct physiological systems may influence each other thereby placing additional strain on the organism. Most studies examining cortisol and BP rhythms tend to look at them in isolation, which obscures potential links. The few studies that do support an association between cortisol and BP (21–23) are limited by small sample sizes and diseased populations or they fail to examine their circadian rhythms. Therefore, the primary aim of this study was to directly examine this potential link. Given that cortisol and BP are both related to stress and that elevated evening cortisol is related to increased arousal and disrupted sleep (13,24), it was hypothesized that a lack of a drop in cortisol from day to night would be associated with decreased BP dipping. As an ancillary aim, we were also interested in examining the relative importance of age and normotensive versus prehypertensive status in moderating such an association.


   METHOD
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Participants
To test the hypotheses, 301 healthy adults aged 20 to 68 years (mean ± standard deviation = 31.16 ± 9.82) were recruited. The sample consisted of 146 males and 155 females, primarily Caucasian (82%) (also, Hispanic 6.7% and Asian 4.3%), and educated (16.41 years of education). Consistent with prior research (25), the following self-reported inclusion criteria were used to select healthy participants: no existing hypertension, no cardiovascular prescription medication use, no past history of chronic disease with a cardiovascular (e.g., diabetes) or immune (e.g., cancer) component, no recent history of psychological disorder (e.g., major depressive disorder), and no consumption of >10 alcoholic beverages a week. Participants were also excluded if they were taking steroids or were pregnant.

Procedures
Subjects volunteered to participate in a 24-hour study in which ambulatory BP was monitored and salivary cortisol was obtained. The data were collected over 1.5-year period between 2003 and 2005 and were approved by the Institutional Review Board/Ethics Committee at Brigham Young University. Interested participants were first screened over the phone to determine if they met the inclusion criteria. Qualified participants were scheduled to come into the laboratory on week days (Monday through Friday) to standardize the impact of a work day versus nonwork day. At the laboratory (after consent was obtained), participants completed a packet of questionnaires that assessed standard variables that may influence health (e.g., demographics, health history). Height and weight were obtained on a standard medical scale (e.g., Health-O-Meter) to ensure accurate measurements of body mass index (BMI). Three baseline clinical BP measurements were taken using a sphygmomanometer and stethoscope. Participants were then given instructions for ambulatory monitoring and a trained research assistant placed the monitors on the subjects. For validation purposes, a minimum of three readings from the ambulatory monitor were compared against those readings obtained from a sphygmomanometer using a T-tube adapter. Readings were considered valid if three consecutive readings matched (±5 mm Hg). After the BP validation procedure, participants received verbal and written instructions on saliva collection. A saliva sample was taken to ensure they knew how to properly collect the saliva and to obtain a morning sample. Each participant was asked to collect saliva four additional times during the next 24 hours. Thus, a total of five salivary cortisol samples were obtained throughout the 24-hour period. After the participants left the laboratory, they continued to wear the ambulatory BP monitor throughout the day and night as they carried out their normal activities. They returned to the laboratory 24 hours later.

Questionnaires

Background Questionnaire
The questionnaire was designed to assess the basic demographics of our sample. It included items such as age, gender, ethnicity, marital status, income, and religious activity.

Sleep Quality
Participants completed the Pittsburgh Sleep Quality Inventory, a standard self-report measure that assesses sleep quality, latency, duration, efficiency, and disturbances over the past month. It has been found to have good internal consistency, test-retest reliability, and validity (26). In addition, participants were asked to rate their sleep quality that night as compared with an ordinary night by using a 1- to 5-point scale (1 = much worse than usual; 5 = much better than usual). Because sleep disturbance may account for BP dipping, we treated sleep quality as a covariate.

Physiological Measures

Blood Pressure
BP was measured using ambulatory (portable) BP techniques. The Accutracker II (Suntech Medical Instruments, Raleigh, North Carolina) was used to estimate ambulatory readings of systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR). The Accutraker II was designed specifically for ambulatory assessments and is well validated; the readings correspond with intra-arterial BP assessments during rest, isometric exercise, and bicycle exercise (27,28). Importantly, ambulatory monitors are reportedly accurate in assessing nocturnal BP dipping when compared with intra-arterial BP measurements (29). The monitor was set to randomly take a reading approximately every 20 minutes during the day or waking hours (6AM–10:59 PM) and every hour during the night (11 PM–6 AM).

The Accutraker II uses a number of codes that may signify problems with the estimation of the ambulatory cardiovascular assessment. Based on prior research (30), we deleted readings associated with test codes 2 (weak Korotkoff sounds), 3 (microphone difficulties), and 7 (air leaks). Outliers associated with artifactual readings were also identified using the criteria by Marler and colleagues (31). These criteria included: a) SBP < 70 mm Hg or >250 mm Hg; b) DBP < 45 mm Hg or >150 mm Hg; c) HR < 40 beats/minute or >200 beats/minute; and d) SBP/DBP < [1.065 + (0.00125 x DBP)] or >3.0.

According to the National Heart, Lung, and Blood Institute (NHLBI), the risk of cardiovascular disease begins at 115/75 mm Hg and doubles with each increment of 20/10 mm Hg. Therefore, the NHLBI recommends that patients with an SBP of 120 to 139 mm Hg or a DBP of 80 to 89 mm Hg should be considered as prehypertensive. Classifications used in this study are based on these criteria.

Cortisol
Cortisol was assessed via saliva sampling. This noninvasive method has shown high correlations (r > 0.90) with cortisol from serum and plasma samples (3,32). Consistent with standard salivary sampling procedures, we sampled at standardized times to account for diurnal effects. Samples were obtained by using a standard sampling product (Salivette, Sarstedt, Inc., Newton, North Carolina). Participants were instructed to suck or chew on a cotton roll until it was saturated (very soggy—usually about 2 to 3 minutes, 1 minute minimum). The cotton roll was then placed inside a retainer and then in the centrifuge tube. Samples were obtained at 7AM, 12 noon, 5 PM, 10 PM, and on wakening, before the subjects got out of bed. Participants were instructed to record the exact time of each sample collection.

To minimize any potential contamination, we gave the participants the following instructions. Participants were told not to eat a major meal within 60 minutes before sample collection, to avoid alcohol for 24 hours before sample collection, and to avoid dairy products 30 minutes before sample collection. We also informed them to be careful about acidic or high-sugar foods; ideally, they should rinse their mouths thoroughly with water 10 minutes before giving a sample to minimize the potential for saliva contamination. To avoid potential blood contamination, we also recommended that they not brush their teeth within 3 hours before sample collection.

Saliva samples were stored in a freezer (–20°C) until shipped for assay. Salivary cortisol was measured with a commercial immunoassay with chemiluminescence detection (CLIA, IBL-Hamburg, Germany). The assay has a lower detection limit of 0.1 nmol/L with intra- and interassay coefficients of variations <8%.

Statistical Analysis
The primary aim of this study was to test if changes in salivary cortisol predicted ambulatory BP dipping. To assess cortisol circadian rhythm, we examined area under the curve (AUC), a commonly used method in endrocrinological studies to assess circadian rhythms. We followed published guidelines (33) and used the formula for AUC with respect to ground (AUCG), which represents total hormone concentration. Nocturnal dipping was calculated by means of the change score—i.e., taking the average of the BP readings obtained during the day (6 AM–11 PM) and subtracting the average of the nighttime readings (11 PM–6 AM) (14–16). Thus, higher scores indicate more dipping.

Separate simultaneous regression analyses were used to examine the prediction of diurnal salivary cortisol, the statistical interaction between cortisol and age, and the interaction between cortisol and prehypertensive status for each BP dipping outcome (SBP and DBP dipping). Simultaneous regression was used to determine the extent to which variables predict the outcome (BP dipping) and their relative importance (34). A power analysis was conducted to estimate the sample size needed. Based on the models, we hypothesized that the sample size was approximately 200. Thus, our sample size exceeds this and we have sufficient power to analyze our hypotheses.

Covariate selection was determined by identifying factors known to independently contribute to BP or cortisol that could potentially confound the results. We identified and entered into the model and thus statistically controlled for gender, BMI, age, phase of menstrual cycle, sleep quality, morning cortisol, and daytime measures of the relevant cardiovascular assessments. Complete data across all variables were obtained from 230 of our participants.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
DISCUSSION
 NOTES
 REFERENCES
 
Preliminary Analyses
We first ran a series of descriptive statistics. Sample characteristics, presented by normotensive and prehypertensive groupings, are shown in Table 1.


View this table:
[in this window]
[in a new window]

  		TABLE 1. Sample Characteristics Reported in Frequency and Mean ± Standard Deviation Values

 

Before testing our primary hypothesis, we examined if our saliva sampling protocol had been followed properly. On inspection, we found that 12 (3.9%) of our 301 participants failed to provide all five saliva samples. Of these, only three (<1%) were missing >1 of 5 samples. Of those with complete data, it is important to know if these samples were taken at appropriate times to assess diurnal variation. Compliance, determined by comparing the instructed sample collection time against the participant’s recorded time, was calculated as the number of compliant samples divided by the total number of samples. Because the first morning sample was scheduled and taken in the laboratory, these samples were all considered compliant. Consistent with research (35), daytime samples were considered compliant if they were ±60 minutes of the instructed sampling time and waking samples were considered compliant if they were within ±15 minutes of awakening. On inspection, we found that 5.6% of samples did not have a recorded time associated with them and 3% were not taken at the correct times. To be conservative, we assumed that those with no recorded time were not compliant with the time we specified. Therefore, our overall study compliance was 91%.

Does Diurnal Variation Salivary Cortisol Predict BP Dipping?
Results indicated that diurnal variation in cortisol, as measured by AUCG, was a significant predictor of BP dipping.1 The relationship was ß = –0.31, p < .0001 for SBP, and ß = –0.37, p < .0001 for DBP. Thus, the less cortisol changed, the less BP dipped at night. The cortisol AUC also had a larger standardized ß than any of the covariates, including BMI.

Does Prediction of BP Dipping Depend on Age?
Advancing age has been identified in the literature as being associated with decreased dipping in both men and women (36). Consistent with the literature, we found that age did predict dipping for both SBP (ß = –0.18, p = .003) and DBP (ß = 0.14, p = .02). We next tested the interaction between age and cortisol to determine if the association of cortisol and BP dipping differs as a function of age. Regardless of whether we treated age continuously or dichotomously (young = <40 years; older = >40 years), we found no significant interaction effect (age x cortisol) on the prediction of BP dipping. Thus, diurnal cortisol variation predicts nocturnal BP dipping regardless of age.

Does Prediction of BP Dipping Depend on Prehypertensive Status?
Given that much of the literature examines nocturnal BP dipping among hypertensive patients, we examined if the effects seem to differ according to classification of prehypertension. Regardless of whether classification of prehypertensive status was based on clinic or daytime ambulatory BP, prehypertensive status did not predict nocturnal BP dipping. Likewise, there was no significant interaction between prehypertensive status and cortisol for SBP or DBP dipping. Thus, cortisol diurnal variation predicts nocturnal dipping regardless of prehypertensive status.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
NOTES
 REFERENCES
 
The primary aim of this study was to examine a potential link between diurnal cortisol variation and ambulatory BP dipping. Evidence indicates that decreased diurnal variation in cortisol is associated with decreased diurnal variation in BP (or decreased nocturnal dipping). Importantly, these effects are independent of the effect of gender, age, BMI, phase of menstrual cycle, sleep quality, morning cortisol, and daytime BP. Results also demonstrate that the association between cortisol variation and BP dipping is not moderated by age or prehypertensive status. Importantly, we were able to identify this association among a large healthy sample of adults, ranging in age and balanced for gender.

Given that prior research has primarily examined BP dipping among hypertensive patients, older adults, or both (16,18,37), it is unclear the extent to which a lack in nocturnal dipping may be health relevant among young healthy adults. Data from Parati and colleagues (38) suggested that lack of nocturnal BP dipping among normotensive young adults may be indicative of future cardiovascular risk. Importantly, evidence from large prospective studies indicated that, for each 5% increment in the dipping ratio (i.e., nocturnal BP/diurnal BP), there is a 20% to 30% increase in cardiovascular morbidity and mortality (20,39,40). Thus, the health relevance of data from young healthy adults should not be dismissed. Nevertheless, longitudinal studies will be necessary to clarify the extent of long-term health significance.

It is important to acknowledge some potential limitations to this study. First, we only sampled over 1 day. Research indicated that there are individual differences in the extent to which people’s diurnal cycles are consistent (41–43). Also, because we did not sample over multiple days, we cannot determine a causal direction. Likewise, we only sampled BP hourly during the night; a more frequent sampling protocol could increase accuracy. Therefore, future research would be wise to assess more frequently over multiple days to draw firm conclusions. Second, our sample population was predominantly white and educated. Research on nocturnal BP dipping indicates significant differences based on race (12,14,44–46) and SES (47,48). Therefore, the extent to which our sample is generalizable is yet to be determined. Third, we relied on self-report to determine compliance with salivary cortisol sampling. Although compliance with our protocol was high, it is possible that self-reported compliance may be overestimated (35). Finally, this was a cross-sectional study using healthy subjects. Prospective studies, including equal distributions of normotensive, prehypertensive, and hypertensive subjects, may help us better understand the long-term health consequences.

Overall, we believe these findings may have important implications. Our data are consistent with models that argue physiologic systems are interdependent. These systems are coordinated and over time can lead to dysregulation. For instance, central corticotropin-releasing hormone can activate both the automatic nervous system and HPA axis (49) and stimulates the release of ß endorphins (50) and, hence, may initially coordinate the patterning. However, it is possible that over time there is difficulty in turning off the cortisol response (51). In addition, reciprocal associations exist between more peripheral physiological processes and central pathways (52). The complexities of these responses and the conditions under which they may be coordinated are currently being investigated (3,53). Thus, these physiological responses, so closely responsive to psychosocial factors including stress, may affect the body in multiple ways that are interdependent. For instance, neuroendocrine rhythms have the potential to modulate the autonomic control of BP, potentially triggering the onset of cardiovascular events. There is also the potential for autonomic control of BP to modulate neuroendocrine rhythms. An integrative understanding of such processes may be important to identify common (potentially modifiable) pathways as well as reconcile inconsistencies in prior research (e.g., protective/damaging effects). Future studies will benefit from examining how these two variables interact in predicting disease outcomes.

We thank Brandon Jones, Shayna Ernhofer, Laura Cummings, Chad Jenson, Adam Howard, Wendy Birmingham, Brian Mead, and Britta Thunnell for their help running participants through the protocol.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 NOTES
REFERENCES
 
1This finding was also significant when assessing diurnal variation through a change score (morning cortisol – nighttime cortisol) and AUC with respect to increase. Back

This research was generously supported by Grant R0502042 from the Marchionne Foundation and a grant from the Family Studies Center at Brigham Young University (J.H.-L.).

Received for publication June 5, 2006; revision received January 17, 2007.

DOI:10.1097/PSY.0b013e318050d6cc


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 

  1. Chernow B, Alexander HR, Smallridge RC, Thompson WR, Cook D, Beardsley D, Fink MP, Lake CR, Fletcher JR. Hormonal responses to graded surgical stress. Arch Intern Med 1987;147:1273–8.[Abstract/Free Full Text]
  2. Posener JA, Schildkraut JJ, Samson JA, Schatzberg AF. Dirunal variation of plasma cortisol and homovanillic acid in healthy subjects. Psychoneuroendocrinology 1996;21:33–8.[CrossRef][Medline]
  3. Kirschbaum C, Hellhammer DH. Salivary cortisol in psychobiological research: an overview. Neuropsychobiology 1989;22:150–69.[Medline]
  4. Yehuda R, Teicher MH, Trestman RL, Levengood RA, Siever LJ. Cortisol regulation in posttraumatic stress disorder and major depression: a chronobiological analysis. Biol Psychiatry 1996;40:79–88.[CrossRef][Medline]
  5. Rosmond R, Dallman MF, Bjorntorp P. Stress-related cortisol secretion in men: relationships with abdominal obesity and endocrine, metabolic and hemodynamic abnormalities. J Clin Endocrinol Metab 1998;83:1853–9.[Abstract/Free Full Text]
  6. Adam E, Gunnar M. Relationship functioning and home and work demands predict individual differences in diurnal cortisol patterns in women. Psychoneuroendocrinology 2001;26:189–208.[CrossRef][Medline]
  7. Caplan RD, Cobb S, French, JRP. White collar work load and cortisol: Disruption of a circadian rhythm by job stress? J Psychosom Res 1979;23:181–92.[CrossRef][Medline]
  8. Grossi G, Perski A, Lundberg U, Soares J. Associations between financial strain and the diurnal salivary cortisol secretion of long-term unemployed individuals. Integr Physiol Behav Sci 2001;36:205–19.[Medline]
  9. Ockenfels MC, Porter L, Smyth J, Kirschbaum D, Hellhammer DH, Stone AA. Effect of chronic stress associated with unemployment on salivary cortisol: overall cortisol levels, diurnal rhythm, and acute stress reactivity. Psychosom Med 1995;57:460–7.[Abstract]
  10. Loredo JS. Sleep quality and blood pressure dipping in normal adults. Sleep 2004;27:1097–103.[Medline]
  11. Fallo F, Barzon L, Rabbia F, Navarrini C, Conterno A, Veglio F, Cazzaro M, Fava GA, Sonino N. Circadian blood pressure patterns and life stress. Psychother Psychosom 2002;71:350–6.[CrossRef][Medline]
  12. Ituarte PHG, Kamarck TW, Thompson HS, Bacanu S. Psychosocial mediators of racial differences in nighttime blood pressure dipping among normotensive adults. Health Psychol 1999;18:393–402.[CrossRef][Medline]
  13. Septhon SE, Sapolsky RM, Kraemer HC, Spiegel D. Diurnal cortisol rhythm as a predictor of breast cancer. J Natl Cancer Inst 2000;92:994–1000.[Abstract/Free Full Text]
  14. Fumo MT, Teeter S, Lang RM, Bednarz J, Sareli P, Murphy MB. Diurnal blood pressure variation and cardiac mass to American blacks and whites and South African blacks. Am J Hypertens 1992;5:111–6.[Medline]
  15. Sihm I, Shroeder AP, Aalkjaer C, Holm M, Morn B, Mulvany M, Thygesen K, Lederballe O. The relation between peripheral vascular structure, left ventricular hypertophy, and ambulatory blood pressure in essential hypertension. Am J Hypertens 1995;8:987–96.[CrossRef][Medline]
  16. Timio M, Venanzi S, Lolli S, Lippi G, Verdura C, Monarca C, Guerrini E. "Non-dipper" hypertensive patients and progressive renal insufficiency: a 3-year longitudinal study. Clin Nephrol 1995;43:382–7.[Medline]
  17. Kario K, Matsuo T, Kobayashi H, Imiya M, Matsuo M, Shimada K. Nocturnal fall of blood pressure and silent cerebrovascular damage in elderly hypertensive patients: advanced silent cerebrovascular damage in extreme dippers. Hypertension 1996;27:130–5.[Abstract/Free Full Text]
  18. Verdecchia P, Schillaci G, Borgioni C, Ciucii A, Sacchi N, Battistelli M, Guerrieri M, Comparato E, Porcellati C. Gender, day-night blood pressure changes, and left ventricular mass in essential hypertension: dippers and peakers. Am J Hypertens 1995;8:193–6.[CrossRef][Medline]
  19. Ohkubo T, Imai Y, Tsuji I, Nagai K, Watanabe N, Minami N, Kato J, Kikuchi N, Niishiyam A, Aihara A, Sekino M, Satoh H, Hismichi S. Relation between nocturnal decline in blood pressure and mortality. Am J Hypertens 1997;10:1201–7.[CrossRef][Medline]
  20. Ohkubo T, Hozawa A, Yamajuchi J, Kikuya M, Ohmori K, Michimata M, Matsubara M, Hashimoto J, Hoshi H, Araki T, Tsuji I, Satoh H, Hisamichi S, Imai Y. Prognostic significance of the nocturnal decline in blood pressure in individuals with and without high 24-h blood pressure: the Ohasama study. J Hypertens 2002;20:2183–9.[CrossRef][Medline]
  21. Parlapiano C, Borgia MC, Minni A, Alessandri N, Basal I, Saponara M. Cortisol circadian rhythm and 24-hour Holter arterial pressure in OSAS patients. Endocr Res 2005;31:371–4.[CrossRef][Medline]
  22. Piovesan A, Panarelli M, Terzolo M, Osella G, Matrella C, Paccotti P, Angeli A. 24-hour profiles of blood pressure and heart rate in Cushing’s syndrome: relationship between cortisol and cardiovascular rhythmicities. Chronobiol Int 1990;7:263–5.[Medline]
  23. Ahmed N, de la Torre B, Wahlgren NG. Salivary cortisol, a biological marker of stress, is positively associated with 24-hour systolic blood pressure in patients with acute ischaemic stroke. Cerebrovasc Dis 2004;18:206–13.[CrossRef][Medline]
  24. Van Cauter E, Leproult R, Kupfer DJ. Effects of gender and age on the levels and circadian rhythmicity of plasma cortisol. J Clin Endocrinol Metab 1996;81:2468–73.[Abstract]
  25. Cacioppo JT, Malarkey W, Kiecolt-Glaser JK, Uchino BN, Sgoutas-Emch SA, Sheridan JF, Berntson GG, Glaser R. Heterogeneity in neuroendocrine and immune responses to brief psychological stressors as a function of autonomic cardiac activation. Psychosom Med 1995;57:154–64.[Abstract/Free Full Text]
  26. Buysse DJ, Reynolds CF, Monk TH, Berman SR, Kupfer DJ. The Pittsburgh sleep quality index: a new instrument for psychiatric practice and research. Psychiatry Res 1989;28:193–213.[CrossRef][Medline]
  27. White WB, Lund-Johansen P, Omvik P. Assessment of four ambulatory blood pressure monitors and measurements by clinicians versus intraarterial blood pressure at rest and during exercise. Am J Cardiol 1990;65:60–6.[Medline]
  28. Light KC, Obrist PA, Cubeddu LX. Evaluation of a new ambulatory blood pressure monitor (Accutraker 102): Laboratory comparisons with direct arterial pressure, stethoscopic ausculatory pressure, and readings from a similar monitor (Spacelabs model 5200). Psychophysiology 1988;25:107–16.[Medline]
  29. Villani A, Parati G, Groppelli A, Ombon S, Di Renzo M, Mancia G. Noninvasive automatic blood pressure monitoring does not attenuate nighttime hypotension: evidence from 24 h intraarterial blood pressure monitoring. Am J Hypertens 1992;5:744–7.[Medline]
  30. Kamarck TW, Shiffman SM, Smithline L, Goodie JL, Paty JA, Gnys M, Yi-Kuan JJ. Effects of task strain, social conflict, and emotional activation on ambulatory cardiovascular activity: daily life consequences of recurring stress in a multiethnic adult sample. Health Psychol 1998;17:17–29.[CrossRef][Medline]
  31. Marler MR, Jacob RG, Lehoczky JP, Shapiro AP. The statistical analysis of treatment effects in 24-hour ambulatory blood pressure recordings. Stat Med 1988;7:697–716.[Medline]
  32. Kirschbaum C, Hellhammer DH. Salivary cortisol in psychoneuroendocrine research: recent developments and applications. Psychoneuroendocrinology 1994;19:313–33.[CrossRef][Medline]
  33. Pruessner JC, Kirschbaum C, Meinlschmid G, Hellhammer DH. Two formulas for computation of area under the curve represents measures of total hormone concentration versus time dependent change. Psychoneuroendrinology 2003;28:916–31.[CrossRef]
  34. Keith TZ. Multiple regression and beyond. Boston: Allyn & Bacon; 2006.
  35. Broadrick JE, Arnold D, Kudielka BM, Kirschbaum C. Salivary cortisol sampling compliance: comparison of patients and healthy volunteers. Psychoneuroendocrinology 2004;29:636–50.[CrossRef][Medline]
  36. Staessen JA, Thijs L, Fagard R, O’Brien ET, Clement D, de Leeuw PW, Mancia G, Nachev C, Palatini P, Parati G, Tuomilehto J, Webster J. Predicting cardiovascular risk using conventional vs ambulatory blood pressure in older patients with systolic hypertension. JAMA 1999;282:539–46.[Abstract/Free Full Text]
  37. Muiesan ML, Pasini G, Salvetti M, Calebich S, Zulli R, Castellano M, Rizzoni D, Bettoni G, Cinelli A, Porteri E, Corsetti V, Agabiti-Rosei E. Cardiac and vascular structural changes. Prevalence and relation to ambulatory blood pressure in a middle-aged general population in Northern Italy: the Vobarno study. Hypertension 1996;27:1046–52.[Abstract/Free Full Text]
  38. Parati G, Ravogli A, Giannattasio C, Mutti E, Trazzi S, Villani A, Mancia G. Changes in 24 hour blood pressure and in cardiac and vascular structure in normotensive subjects with parental hypertension. Clin Exp Hypertens A 1992;14:67–83.[Medline]
  39. Verdecchia P, Porcellati C, Schillaci G, Borgioni C, Ciucci A, Battistelli, M, Guerrieri M, Gatteschi C, Zamipi I, Santucci A. Ambulatory blood pressure: An independent predictor of prognosis in essential hypertension. Hypertension 1994;24:793–801.[Abstract/Free Full Text]
  40. Verdecchia P, Schillaci G, Borioni C, Ciucci A, Gattobigio R, Porcellati C. Nocturnal pressure is the true pressure. Blood Press Monitor 1996;1:S81–5.
  41. Smyth JM, Ockenfels MC, Gorin AA, Catley D, Porter LS, Kirschbaum C, Hellhammer DH, Stone AA. Individual differences in the diurnal cycle of cortisol. Psychoneuroendocrinology 1997;22:89–105.[CrossRef][Medline]
  42. Mochizuki Y, Okutani M, Donfeng Y, Iwasaki H, Takusagawa M, Kohno I, Mochizuki S, Umetani K, Ishii H, Ijiri H, Komori S, Tamura K. Limited reproducibility of circadian variation in blood pressure dippers and nondippers. Am J Hypertens 1998;11:403–9.[CrossRef][Medline]
  43. Manning G, Rushton L, Donnelly R, Millar-Draig MW. Variability of diurnal changes in ambulatory blood pressure and nocturnal dipping status in untreated hypertensive and normotensive subjects. Am J Hypertens 2000;13:1035–8.[CrossRef][Medline]
  44. Profant J, Dimsdale JE. Race and diurnal blood pressure patterns. A review and meta-analysis. Hypertension 1999;33:1099–104.[Abstract/Free Full Text]
  45. Herbert LA, Agarwal G, Ladson-Wafford SE, Reif M, Hiremath L, Carlton SG, Nahman NS, Falkenhain ME, Agarwal A. Nocturnal blood pressure in treated hypertensive African Americans compared to treated hypertensive European Americans. J Am Soc Nephrol 1996;7:2130–4.[Abstract]
  46. Gretler DD, Eumo MT, Nelson KS, Murphy MB. Ethnic differences in circadian hemodynamic profile. Am J Hypertens 1994;7:7–14.[Medline]
  47. Stepnowsky CJ, Nelesen, RA, DeJardin D, Dimsdale JE. Socioeconomic Status is associated with nocturnal blood pressure dipping. Psychosom Med 2004;66:651–5.[Abstract/Free Full Text]
  48. Cohen S, Schwarz J, Epel E, Kirschbaum C, Sidney S, Seeman T. socioeconomic status, race, and diurnal cortisol decline in the coronary artery risk development in young adults (CARDIA) study. Psychosom Med 2006;68:41–50.[Abstract/Free Full Text]
  49. Irwin M. Stress-induced immune suppression: role of brain corticotropin releasing hormone and autonomic nervous system mechanisms. Adv Neuroimmunol 1994;4:29–47.[Medline]
  50. Rivier C, Brownstein M, Spiess J, Rivier J, Vale W. In vivo corticotropin-releasing factor-induced secretion of adrenocorticotropin, beta-endorphin, and corticosterone. Endocrinology 1982;110:272–8.[Abstract/Free Full Text]
  51. Seeman TE, Singer B, Charpentier P. Gender differences in patterns of HPA axis response to challenge: Macarthur studies of successful aging. Psychoneuroendocrinology 1995;20:711–25.[CrossRef][Medline]
  52. Maier SF, Watkins LR, Fleshner M. Psychoneuroimmunology. The interface between behavior, brain, and immunity. Am Psychol 1994;49:1004–17.[CrossRef][Medline]
  53. Dunn AJ, Berridge CW. Physiological and behavioral responses to corticotropin-releasing factor administration: is CRF a mediator of anxiety or stress responses? Brain Res Brain Res Rev 1990;15:71–100.[CrossRef][Medline]




This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Holt-Lunstad, J.
Right arrow Articles by Steffen, P. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Holt-Lunstad, J.
Right arrow Articles by Steffen, P. R.
Related Collections
Right arrow Endocrinology
Right arrow Neuroendocrine
Right arrow Psychophysiology
Right arrow Sleep and Biological Rhythms
Right arrow Blood Pressure

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS