Psychosomatic Medicine Tips for Better Browsing
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Abstract Freely available
Right arrow Figures Only
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bardwell, W. A.
Right arrow Articles by Dimsdale, J. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bardwell, W. A.
Right arrow Articles by Dimsdale, J. E.
Related Collections
Right arrow Endocrinology
Right arrow Nutrition
Right arrow Psychophysiology
Psychosomatic Medicine 62:569-575 (2000)
© 2000 American Psychosomatic Society

ORIGINAL ARTICLES

Influence of Cholesterol and Fasting Insulin Levels on Blood Pressure Reactivity

Wayne A. Bardwell, PhD, Michael G. Ziegler, MD and Joel E. Dimsdale, MD

From the Departments of Psychiatry (W.A.B., J.E.D.) and Medicine (M.G.Z.), University of California, La Jolla; and Veterans Affairs San Diego Healthcare System (W.A.B.), San Diego, CA.

Address reprint requests to: Joel Dimsdale, MD, University of California, San Diego, La Jolla, CA 92093-0804. Email: jdimsdale{at}ucsd.edu


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
OBJECTIVE: This study examined how cholesterol and fasting insulin levels are related to blood pressure reactivity to behavioral stressors.

METHODS: Subjects (N = 116) were 20 to 52 years old, at 80% to 150% of ideal weight, and had an average fasting cholesterol level of 183 mg/dl. Stressor tasks included mirror star tracing and a videotaped speech task. Changes from baseline were calculated for systolic and diastolic blood pressure.

RESULTS: Neither cholesterol nor insulin was independently related to blood pressure change scores. However, after controlling for body mass, a two-way analysis of variance revealed a significant cholesterol-by-insulin interaction for change in diastolic blood pressure (p = .022). Subjects in the high-cholesterol/high-insulin group showed the greatest increase in diastolic blood pressure reactivity.

CONCLUSIONS: In a general population, people with a below-average cholesterol level experience only moderate cardiovascular reactivity to mental stressors regardless of their fasting insulin level. However, for people with an above-average cholesterol level, fasting insulin level is an important factor in determining potential reactivity to mental stressors. These findings highlight the importance of adequate sample size to allow for the analysis of such interactions in future studies of cholesterol, insulin, and blood pressure reactivity.

Key Words: cardiovascular reactivity • blood pressure • cholesterol • insulin

Abbreviations: ANOVA = analysis of variance; BMI = body mass index; BP = blood pressure; CVR = cardiovascular reactivity; DBP = diastolic blood pressure; HR = heart rate; NO =nitric oxide; SBP = systolic blood pressure.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
The study of CVR is a growing field. Documenting variability in reactivity among people is interesting in its own right, and some evidence suggests that increased reactivity predicts future illness or is associated with current illness (1–5).

Considerable effort is spent on identifying variables related to increased reactivity. In social psychological studies, the presence of social support has been shown to attenuate SBP (6–10), DBP (7, 9–12), and HR (7) reactivity to psychological stressors. In personality studies, conflicting results have been found regarding relationships between CVR and such personality traits as hostility (13–15) and anger expression (16–22).

In physiological studies, the diagnosis of hypertension seems to be related to increased CVR (23–29). Several researchers have found links between lipid levels and CVR (30–39), whereas others have not (40, 41). Also, relationships between insulin levels and CVR have been documented (28, 42–48). Syndrome X is a composite coronary vascular disease risk profile consisting of increased lipids, insulin resistance, hypertension, and alterations in BMI (49). This area of research is interesting to psychiatrists and behavioral medicine researchers because these variables are influenced by behavior. Research that explores relationships between CVR and syndrome X variables may have significant implications for the identification of patients who can benefit most from medical and behavioral interventions and in deciding the best course of treatment for a particular patient.

The focus of this article is the relationship between BP reactivity and both lipid and fasting insulin levels. Several researchers have demonstrated that lipid levels are positively correlated with BP and/or HR reactivity to a variety of mental stressor tasks (30–35, 38, 39). Other researchers have found similar positive relationships between insulin levels and BP and/or HR reactivity to stressor tasks (28, 42, 45, 47, 48). We wondered whether people with both high cholesterol and high insulin levels would show an even greater proclivity for hyperreactivity. Table 1 summarizes results reported from studies of lipids vs. BP reactivity and insulin vs. BP reactivity to mental stressor tasks. Of the 10 lipid vs. reactivity studies, five reported significant positive correlations between SBP and lipids, three reported significant positive correlations between DBP and lipids, and five reported significant positive correlations between HR and lipids. Two significant negative correlations were also reported, one each for DBP and HR. Of the five insulin vs. reactivity studies in Table 1, two reported significant positive correlations between SBP and insulin, two reported significant positive correlations between DBP and insulin, and one reported significant positive correlations between HR and insulin. Also, one study reported a significant negative correlation between DBP and insulin.


View this table:
[in this window]
[in a new window]
  		Table 1. Research Summary: Cholesterol and Insulin vs. BP and HR Reactivity to Mental Stressorsa
 
To confound the problem of dissimilar findings, many of the studies listed in Table 1 had a limited sample size. Excluding the large study by van Doornen et al. (38), the mean sample size of these studies is 52. In addition, the generalizability of research results frequently depends on subject selection. In one study, subjects in the high-cholesterol category had diagnosable hypercholesterolemia (35), whereas in two other studies, subjects in the high-insulin group had a diagnosis of non–insulin-dependent diabetes mellitus (28, 48). Other studies looked at these relationships in women only (7, 11, 13, 14, 16, 33, 42), young men (17, 19, 21–23, 41, 44, 45), recent myocardial infarction patients (40), physicians and dentists (32), and students (7–10, 13–16, 18, 19, 21–23, 41).

Because of these sample characteristics, the generalizability of these findings to broader populations is unsure, and the ability to examine insulin-by-cholesterol interactions has been restricted because of sample size or the apparent unavailability of one or the other of these variables. We were interested in determining whether the reported relationships would hold when a large sample of subjects other than healthy, normotensive students was studied. Therefore, we studied a group of 116 normotensive and hypertensive adults with a range of insulin and cholesterol levels.

The purposes of this study were to replicate previously reported findings of significant independent relationships between cholesterol or fasting insulin level and BP reactivity measures and, because we had the benefit of a large sample, to determine whether there might also be a cholesterol-by-insulin interaction for the BP reactivity measures. We hypothesized that subjects with both high cholesterol and high fasting insulin levels would show greater BP reactivity than subjects with a high level of only one of these metabolic factors or low levels of both.

This hypothesis was based on two important factors. First, insulin and cholesterol have been implicated in the atherosclerotic process. Second, as reported by van Doornen et al. (38), there are at least two possible mechanisms for a relationship between hyperlipidemia and CVR: Heistad et al. (51) found lipid levels to be associated with increased sensitivity to vasoconstrictors, and Casino et al. (52) reported an association between high lipid levels and decreased vascular relaxation. Insulin has both vasodilatory and vasoconstrictive effects. Insulin has vasodilating activity because it stimulates release of NO from vascular endothelial cells. This is greatest in blood vessels supplying muscle and leads to increased blood flow to muscles, where glucose is removed from the bloodstream. Insulin also has vasoconstricting activity by stimulating sympathetic nervous system activity and norepinephrine release. This helps maintain BP and shunts blood from some organs toward muscle. The vasodilating capacity of insulin and the ability of vessels to release NO is impaired in some vascular diseases associated with high cholesterol (52). It is difficult to predict in advance which aspects of insulin’s vascular actions will predominate with various stimuli. We wondered whether subjects with high levels of both lipids and insulin would show the greatest reactivity.

BMI has been shown to have an association with BP separate from those of lipids and insulin (53). Because of its potentially confounding role, we controlled for the effects of weight by using BMI as a covariate.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Volunteers were recruited through community BP screening or word-of-mouth referral. The sample consisted of 116 participants: 68% male and 32% female, 59% white and 41% black, 73% normotensive and 27% hypertensive, 20 to 52 years old. To qualify, subjects had to be 80% to 150% of ideal weight, as determined by Metropolitan Life Insurance tables (54). Subjects were excluded if they had any ongoing major illness other than hypertension. All women were tested during the follicular phase (7–10 days after menses) of the menstrual cycle. Volunteers were studied after we had obtained written informed consent. The protocol was approved by the University of California, San Diego, institutional review board.

BP was measured with a Dinamap 845 XT monitor (Critikon, Inc, Tampa, FL). BP readings obtained from the Dinamap correlate well (r > .95) with mercury sphygmomanometry readings (55). Subjects came to the laboratory for BP screening at their own convenience on two separate occasions approximately 1 week apart. On each visit, after the subject had been seated for at least 5 minutes to acclimate to the equipment, three consecutive readings were taken. Subjects who were taking antihypertensive medication had their medication tapered for 3 weeks before BP screening. Subjects whose SBP while not taking medication was 140 to 180 mm Hg or whose DBP was 90 to 110 mm Hg were considered hypertensive and eligible to participate. Subjects whose SBP was less than 140 mm Hg and whose DBP was less than 90 mm Hg were considered normotensive. Only subjects who remained in the same diagnostic category on both screening occasions were enrolled.

Subjects were studied at 8:30 AM. On arrival at the laboratory, an appropriately sized blood pressure cuff (with a Dinamap monitor) was placed on the nondominant arm, and a 19-gauge catheter was placed for blood sampling. Participants then rested for 30 minutes to become acclimated to the monitoring equipment and testing environment. A 3-minute baseline period followed the resting period.

After the baseline period, participants were given instructions for a speaking task, which required preparing (3 minutes) and delivering (3 minutes) a speech in front of a videocamera (56). They were told that the speech, which involved defending themselves from being falsely accused of shoplifting, would be evaluated and rated by experts. If they stopped speaking before the 3 minutes were up, they were reminded to continue talking by reiterating and summarizing their points. The subjects also participated in a mirror star tracing task. This involves tracing the outline of a star using its mirror image for 3 minutes. The task has been used widely in reactivity standardization paradigms and has been shown to lead to increased BP (57, 58). The two stressor tasks were imposed in random order, and a recovery period of 15 minutes separated the two tasks.

SBP and DBP readings were obtained once per minute during the 3-minute baseline period and during each 3-minute stress task. The readings for each cardiovascular measure were averaged to form separate SBP and DBP values for baseline, speech preparation, speech delivery, and mirror star tracing. Average baseline values were then subtracted from the average for each task to obtain SBP and DBP change scores for each task. Finally, the change scores for each task were averaged for each cardiovascular measure, resulting in one overall mean change score for each BP measure (SBP and DBP). We averaged the change scores for all of the stressor tasks because we wanted to examine overall reactivity rather than draw inferences based on reactivity to only one task. Data were analyzed using ANOVA and regression analysis.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects were divided into high and low groups using median splits on cholesterol (180 mg) and fasting insulin (10 U). For ANOVA models, subjects were categorized into four cholesterol-by-insulin groups based on the median splits: high-cholesterol/high-insulin, high-cholesterol/low-insulin, low-cholesterol/high-insulin, and low-cholesterol/low-insulin. For regression analysis, continuous cholesterol and insulin variables were used as independent variables.

The four cholesterol-by-insulin groups were similar in age and baseline SBP and DBP. Hypertensive subjects were fairly evenly distributed across the groups. However, the groups differed significantly in terms of BMI (p < .001) (Table 2). Because of this, and because BMI has been shown to be related to BP independent of lipid and insulin levels, we controlled for the effects of BMI in all of the analyses.


View this table:
[in this window]
[in a new window]
  		Table 2. Subject Variablesa
 
In the ANOVA, there were no significant main effects for cholesterol or insulin: The high- vs. low-cholesterol and high- vs. low-insulin groups did not differ significantly in terms of mean SBP or DBP change scores. Also, when continuous measures of cholesterol and insulin were used as independent variables, and their product was included as an interaction term, none of the regression models revealed significant relationships with any of the cardiovascular change scores. When two-way ANOVA was performed, results were not significant when mean SBP change scores were used as the dependent variable. When mean DBP change scores were used as the dependent variable in a two-way ANOVA, a significant cholesterol-by-insulin interaction was found (p = .022). A plot of this interaction revealed that subjects with high levels of both cholesterol and fasting insulin experienced the greatest reactivity to stress (Figure 1). Analysis of this interaction showed that, in terms of mean reactivity, the low-cholesterol/low-insulin group did not differ from the low-cholesterol/high-insulin group (p = .754), the high-cholesterol/high-insulin group (p = .387), or the high-cholesterol/low-insulin group (p = .316). Also, the low-cholesterol/high-insulin group did not differ from the high-cholesterol/high-insulin group (p = .295). However, for subjects with a high cholesterol level, those who also had a high insulin level showed significantly greater mean DBP change than those who had a low insulin level (p = .032).



View larger version (29K):
[in this window]
[in a new window]
  		Fig. 1. Cholesterol-by-insulin interaction.

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
ACKNOWLEDGMENTS
 REFERENCES
 
There are many indices of CVR to mental stressor tasks, and the literature is inconsistent regarding their relationships with lipids and insulin. Each index may reflect a somewhat different underlying physiology. It is apparent that findings from recent studies are across the board, with results differing by population and CVR measures used. The studies have a misleading appearance of comparability. In fact, the subject populations differ enormously, ranging from children to adults with diabetes or hypercholesterolemia. Sample size is also a limiting factor in many of the studies, limiting the power to identify other relationships that may exist between lipids or cholesterol and CVR. In addition, none of the studies we came across included analyses of the cholesterol-by-insulin interaction. Because it has been reported that lipid levels are associated with decreased vascular relaxation and increased sensitivity to vasoconstrictors, and because insulin has both vasoconstrictive and vasodilatory effects, we thought this interaction would be important to study.

Using a variety of statistical analysis techniques, we were unable to replicate the previously reported independent relationships between BP and either cholesterol or fasting insulin. Differences in subject selection could at least partially explain this discrepancy in findings, because many of the previous studies relied on medical patients or other specific populations (eg, physicians or students) or had a narrow range of ages. We were interested in determining whether the reported relationships would hold in a broader sample of subjects.

After using median splits on cholesterol and insulin to partition subjects into four groups, a two-way ANOVA resulted in a significant cholesterol-by-fasting insulin interaction with the mean change in DBP. Surprisingly, the low-cholesterol/low-insulin group did not differ from the high-cholesterol/high-insulin group in terms of reactivity. We expected these groups to show a significant difference and are unsure how to explain this discrepancy. However, of the four groups, subjects who were in the high-cholesterol/high-insulin group experienced the greatest mean increase in DBP, an increase significantly higher than that of subjects in the high-cholesterol/low-insulin group.

Results of the regression models, which used continuous cholesterol and insulin measures plus their product as an interaction term, were not significant. We would normally expect a model based on continuous variables to be more sensitive than an ANOVA using dichotomous variables, because most biological effects more nearly approximate a linear function than a nonlinear function. In this case, the data suggest that the product of insulin and cholesterol has a nonlinear relationship with change in DBP. The gain in sensitivity of the regression approach may have been negated by the nonlinear relationship between the interaction term and the change in DBP. Furthermore, the nature of this interaction makes the selection of the cholesterol and insulin cutoff points used in the ANOVAs important. We used median splits on both variables. In a post hoc sensitivity analysis in which we selected various cutoff points that were smaller or larger than the medians, we produced interaction terms that resulted in varying levels of significance (p < .00004 to p = .20). Thus, the results may depend on the choice of threshold, which makes further replication all the more important.

We found no significant relationships for SBP. This suggests that the cardiovascular effects of cholesterol and insulin manifest in terms of peripheral resistance. Although it is possible that our findings are random, they may be informing us about the underlying physiology of cholesterol, insulin, and BP reactivity.

The role of insulin in CVR is complex, because insulin can function as a vasodilator or vasoconstrictor. The ability of insulin to cause vasodilation and the ability of endothelial cells to release NO is impaired in some diseases associated with high cholesterol levels, and this may help explain the findings of this study. In our sample of 116 individuals, what is particularly striking is that the effect of high cholesterol on CVR to mental stressors seems to be influenced by fasting insulin levels. To phrase it another way, insulin seems to affect reactivity only in the presence of high cholesterol. These findings may help explain some of the differences in results reported in the lipid/CVR literature. They may also have clinical implications in understanding cardiovascular disease in patients who are both hypercholesterolemic and insulin-resistant. In addition, these findings highlight the importance of an adequate sample size to allow for the analysis of such interactions in future studies of cholesterol, insulin, and CVR.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
REFERENCES
 
This work was supported by Grants HL36005 and RR00827 from the National Institutes of Health. The authors thank Lorenz van Doornen, PhD, who was action editor for this manuscript.

Received for publication December 28, 1998.

Revision received November 9, 1999.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 

  1. Fredrikson M, Tuomisto M, Bergman-Losman B. Neuroendocrine and cardiovascular stress reactivity in middle-aged normotensive adults with parental history of cardiovascular disease. Psychophysiology 1991; 28: 656–64.[Medline]
  2. Hendrix WH, Hughes RL. Relationship of trait, Type A behavior, and physical fitness variables to cardiovascular reactivity and coronary heart disease risk potential. Am J Health Promotion 1997; 11: 264–71.[Medline]
  3. Jennings JR, Kamarck T, Manuck S, Everson SA, Kaplan G, Salonen JT. Aging or disease? Cardiovascular reactivity in Finnish men over the middle years. Psychol Aging 1997; 12: 225–38.[Medline]
  4. Krantz DS, Helmers KF, Bairey CN, Nebel LE, Hedges SM, Rozanski A. Cardiovascular reactivity and mental stress–induced myocardial ischemia in patients with coronary artery disease. Psychosom Med 1991; 53: 1–12.[Abstract/Free Full Text]
  5. Sundin O, Ohman A, Palm T, Streom G. Cardiovascular reactivity, Type A behavior, and coronary heart disease: comparisons between myocardial infarction patients and controls during laboratory-induced stress. Psychophysiology 1995; 32: 28–35.[Medline]
  6. Christenfeld N, Gerin W, Linden W, Sanders M, Mathur J, Deich JD, Pickering TG. Social support effects on cardiovascular reactivity: is a stranger as effective as a friend? Psychosom Med 1997; 59: 388–98.[Abstract/Free Full Text]
  7. Kamarck TW, Manuck SB, Jennings JR. Social support reduces cardiovascular reactivity to psychological challenge: a laboratory model. Psychosom Med 1990; 52: 42–58.[Abstract/Free Full Text]
  8. Lepore SJ. Cynicism, social support, and cardiovascular reactivity. Health Psychol 1995; 14: 210–6.[Medline]
  9. Uchino BN, Garvey TS. The availability of social support reduces cardiovascular reactivity to acute psychological stress. J Behav Med 1997; 20: 15–27.[Medline]
  10. Lepore SJ, Allen KA, Evans GW. Social support lowers cardiovascular reactivity to an acute stressor. Psychosom Med 1993; 55: 518–24.[Abstract/Free Full Text]
  11. Gerin W, Milner D, Chawla S, Pickering TG. Social support as a moderator of cardiovascular reactivity in women: a test of the direct effects and buffering hypothesis. Psychosom Med 1995; 57: 16–22.[Abstract/Free Full Text]
  12. Gerin W, Pieper C, Levy R, Pickering TG. Social support in social interaction: a moderator of cardiovascular reactivity. Psychosom Med 1992; 54: 324–36.[Abstract/Free Full Text]
  13. Fichera LV, Andreassi JL. Stress and personality as factors in women’s cardiovascular reactivity. Int J Psychophysiol 1998; 28: 143–55.[Medline]
  14. Powch IG, Houston BK. Hostility, anger-in, and cardiovascular reactivity in white women. Health Psychol 1996; 15: 200–8.[Medline]
  15. Shapiro D, Goldstein IB, Jamner LD. Effects of anger/hostility, defensiveness, gender, and family history of hypertension on cardiovascular reactivity. Psychophysiology 1995; 32: 425–35.[Medline]
  16. Anderson SF, Lawler KA. The Anger Recall Interview and cardiovascular reactivity in women: an examination of context and experience. J Psychosom Res 1995; 39: 335–43.[Medline]
  17. Bongard S, al’Absi M, Lovallo WR. Interactive effects of trait hostility and anger expression on cardiovascular reactivity in young men. Int J Psychophysiol 1998; 28: 181–91.[Medline]
  18. Harralson TL, Suarez EC, Lawler KA. Cardiovascular reactivity among hostile men and women: effects of age and anger suppression. Womens Health 1997; 3: 151–64.[Medline]
  19. Hodapp V, Heiligtag U, Steormer SW. Cardiovascular reactivity, anxiety and anger during perceived controllability. Biol Psychol 1990; 30: 161–70.[Medline]
  20. Laude D, Girard A, Consoli S, Mounier-Vehier C, Elghozi, JL. Anger expression and cardiovascular reactivity to mental stress: a spectral analysis approach. Clin Exp Hypertens 1997; 19: 901–11.
  21. Miller SB. Cardiovascular reactivity in anger-defensive individuals: the influence of task demands. Psychosom Med 1993; 55: 78–85.[Abstract/Free Full Text]
  22. Siegman AW, Anderson R, Herbst J, Boyle S, Wilkinson J. Dimensions of anger-hostility and cardiovascular reactivity in provoked and angered men. J Behav Med 1992; 15: 257–72.[Medline]
  23. al’Absi M, Everson SA, Lovallo WR. Hypertension risk factors and cardiovascular reactivity to mental stress in young men. Int J Psychophysiology 1995; 20: 155–60.[Medline]
  24. Cardillo C, Degen C, DeFelice F, Folli G. Effects of celiprolol on cardiovascular reactivity to laboratory stressors in patients with hypertension. Clin Pharmacol Ther 1992; 51: 555–61.[Medline]
  25. DeChamplain J, Petrovich M, Gonzalez M, Lebeau R, Nadeau R. Abnormal cardiovascular reactivity in borderline and mild essential hypertension. Hypertension 1991; 17 (4 Suppl):III22–8.
  26. Falkner B. The role of cardiovascular reactivity as a mediator of hypertension in African Americans. Semin Nephrol 1996; 16: 117–25.[Medline]
  27. Knardahl S, Hendley ED. Association between cardiovascular reactivity to stress and hypertension or behavior. Am J Physiol 1990; 259 (1 Pt 2): J248–57.
  28. Nazzaro P, Merlo M, Manzari M, Mudoni A, Cicco G, Pirrelli A. Diabetes modifies cardiovascular reactivity during hypertension. Am J Med Sci 1994; 307 (Suppl 1): S142–5.
  29. Potempa K. An overview of the role of cardiovascular reactivity to stressful challenges in the etiology of hypertension. J Cardiovasc Nurs 1994; 8: 27–38.[Medline]
  30. Burker EJ, Fredrikson M, Rifai N, Siegel W, Blumenthal JA. Serum lipids, neuroendocrine and cardiovascular responses to stress in men and women with mild hypertension. Behav Med 1994; 19: 155–61.[Medline]
  31. Jorgensen RS, Nash JK, Lasser NL, Hymowitz N, Langer AW. Heart rate acceleration and its relationship to total serum cholesterol, triglycerides, and blood pressure reactivity in men with mild hypertension. Psychophysiology 1988; 25: 39–44.[Medline]
  32. McKinney ME, McIlvain HE, Hofschire PJ, Collins RE, Somers JA, Ruddel H, Buell JC, Eliot RS. Cardiovascular changes during mental stress: correlations with presence of coronary risk factors and cardiovascular disease in physicians and dentists. J Hum Hypertens 1987; 1: 137–45.[Medline]
  33. Owens J, Stoney CM, Matthews KA. Menopausal status influences ambulatory blood pressure levels and blood pressure changes during mental stress. Circulation 1993; 88: 2794–2802.[Abstract/Free Full Text]
  34. Suarez EC, Williams RB, Kuhn CM, Zimmerman BS, Schanberg SM. Biobehavioral basis of coronary-prone behavior in middle-aged men. Part II. Serum cholesterol, the Type A behavior pattern, and hostility as interactive modulators of physiological reactivity. Psychosom Med 1991; 53: 528–37.[Abstract/Free Full Text]
  35. Sung BH, Izzo JL Jr, Wilson MF. Effects of cholesterol reduction on BP response to mental stress in patients with high cholesterol. Am J Hypertens 1997; 10: 592–9.[Medline]
  36. Straznicky NE, Howes LG, Lam W, Louis WJ. Effects of pravastatin on cardiovascular reactivity to norepinephrine and angiotensin II in patients with hypercholesterolemia and systemic hypertension. Am J Cardiol 1995; 15:75: 582–6.
  37. Straznicky NE, Louis WJ, McGrade P, Howes LG. The effects of dietary lipid modification on blood pressure, cardiovascular reactivity and sympathetic activity in man. J Hypertens 1993; 11: 427–37.[Medline]
  38. van Doornen LJ, Snieder H, Boomsma DI. Serum lipids and cardiovascular reactivity to stress. Biol Psychol 1998; 47: 279–97.[Medline]
  39. Fredrikson M, Lundberg U, Tuomisto M. Serum lipid levels and cardiovascular reactivity. J Psychophysiology 1991; 5: 89–95.
  40. Fredrikson M, Blumenthal JA. Lipids, catecholamines, and cardiovascular responses to stress in patients recovering from myocardial infarction. J Cardiopulm Rehabil 1988; 12: 513–7.
  41. Waldstein DR, Polifrone JM, Bachen EA, Muldoon MF, Kaplan JR, Manuck SB. Relationship of cardiovascular reactivity and anger expression to serum lipid concentrations in healthy young men. J Psychosom Res 1993; 37: 249–56.[Medline]
  42. Sung BH, Wilson MF, Izzo JL Jr, Ramirez L, Dandona P. Moderately obese, insulin-resistant women exhibit abnormal vascular reactivity to stress. Hypertension 1997; 30: 848–53.[Abstract/Free Full Text]
  43. Grover A, Padginton C, Wilson MF, Sung BH, Izzo JL Jr, Dandona P. Insulin attenuates norepinephrine-induced venoconstriction: an ultrasonographic study. Hypertension 1995; 25 (4 Pt 2): 779–84.[Abstract/Free Full Text]
  44. Gans RO, Bilo HJ, von Maarschalkerweerd WW, Heine RJ, Nauta JJ, Donker AJ. Exogenous insulin augments in healthy volunteers the cardiovascular reactivity to noradrenaline but not to angiotensin II. J Clin Invest 1991; 88: 512–8.
  45. Moan A, Nordby G, Rostrup M, Eide I, Kjeldsen SE. Insulin sensitivity, sympathetic activity, cardiovascular reactivity in young men. Am J Hypertens 1995; 8: 268–75.[Medline]
  46. Modan M, Halkin H, Almog S, Lusky A, Eshkol A, Shefi M, Shitrit A, Fuchs Z. Hyperinsulinemia: a link between hypertension, obesity and glucose intolerance. J Clin Invest 1985; 75: 809–17.
  47. Nelesen RA, Dimsdale JE, Mills PJ, Ziegler MG. Relationship of insulin, race, and hypertension with hemodynamic reactivity to a behavioral challenge. Am J Hypertens 1995; 8: 12–9.[Medline]
  48. Sung BH, Wilson MF, Izzo JL Jr, Farooq F, Dandona P Troglitazone (insulin sensitizer) not glyburide (sulfonylurea) improves blood pressure response to mental stress in normotensive, Type II diabetes mellitus[abstract]. Circulation 1996; 94 (Suppl): I-215.
  49. Reaven GM. Syndrome X. Blood Press 1992; 4 (Suppl): 13–6.
  50. Heistad DD, Armstrong ML, Marcus ML, Piegors DJ, Mark AL. Augmented responses to vasoconstrictor stimuli in hypercholesteremic and atherosclerotic monkeys. Circ Res 1984; 54: 711–8.[Abstract/Free Full Text]
  51. Casino PR, Crescence M, Kilcoyne M, Quyyumi AA, Hoeg JM, Panza JA. The role of nitric oxide in endothelium-dependent vasodilation of hypercholesteremic patients. Circulation 1993; 88: 2541–7.[Abstract/Free Full Text]
  52. Baron AD. Vascular reactivity. Am J Cardiol 1999; 84 (1A):25J–27J.[Medline]
  53. Niaura R, Banks SM, Ward KD, Stoney CM, Spiro A III, Aldwin CM, Landsberg L, Weiss ST. Hostility and the metabolic syndrome in older males: the Normative Aging Study. Psychosom Med 2000; 62: 7–16.[Abstract/Free Full Text]
  54. Metropolitan Life Foundation. Metropolitan height and weight tables. Stat Bull Metrop Insur Co 1983; 64: 1.
  55. Silas J, Barker A, Ramsay L. Clinical evaluation of Dinamap 845 automated blood pressure recorder. Br Heart J 1980; 43: 202–5.[Abstract/Free Full Text]
  56. Saab PG, Matthews KA, Stoney CM, McDonald RH. Premenopausal and postmenopausal women differ in their cardiovascular and neuroendocrine responses to behavioral stressors. Psychophysiology 1989; 26: 270–80.[Medline]
  57. Hurwitz BS, Nelesen RA, Saab PG, Nagel JH, Spitzer SB, Gellman MD, McCabe PM, Phillips DJ, Schneiderman N. Dynamic cardiovascular processes supporting blood pressure elevation to three behavioral stressors. Biol Psychol 1993; 36: 75–95.[Medline]
  58. Saab PG, Llabre MM, Hurwitz BE, Frame CA. Myocardial and peripheral vascular responses to behavioral challenges and their stability in black and white Americans. Psychophysiology 1992; 29: 384–97.[Medline]



This article has been cited by other articles:


Home page
 Psychosom. Med.Home page
S. C. Matthews, R. A. Nelesen, and J. E. Dimsdale
Depressive Symptoms Are Associated With Increased Systemic Vascular Resistance to Stress
Psychosom Med, July 1, 2005; 67(4): 509 - 513.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bardwell, W. A.
Right arrow Articles by Dimsdale, J. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bardwell, W. A.
Right arrow Articles by Dimsdale, J. E.
Related Collections
Right arrow Endocrinology
Right arrow Nutrition
Right arrow Psychophysiology

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS