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Psychosomatic Medicine 65:582-587 (2003)
© 2003 American Psychosomatic Society

ORIGINAL ARTICLES

Hostility, Social Support, and Adrenergic Receptor Responsiveness Among African-American and White Men and Women

Joel W. Hughes, PhD, Andrew Sherwood, PhD, James A. Blumenthal, PhD, Edward C. Suarez, PhD and Alan L. Hinderliter, MD

From Department of Psychiatry and Behavioral Sciences (J.W.H., A.S., J.A.B., E.C.S.), Duke University Medical Center, Durham; Department of Medicine (A.L.H.) at the University of North Carolina, Chapel Hill, North Carolina

Address reprint requests to: Andrew Sherwood, PhD, Duke University Medical Center, MC-3119, Durham, NC 27710. Email: sherw002{at}mc.duke.edu

Received for publication March 6, 2002; revision received August 22, 2002.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
OBJECTIVE: We examined the relationship between ß-adrenergic receptor responsiveness and hostility and social support in African American and white men and women.

METHODS: The participants were 149 men and women, aged 25 to 45 years with SBP < 160 and DBP < 105. Hostility and social support were assessed with standardized self-report measures. An isoproterenol challenge was used to evaluate ß-adrenergic receptor responsiveness, and a phenylephrine challenge was used to evaluate {alpha}-adrenergic receptor responsiveness.

RESULTS: Hostility and social support were unrelated to {alpha}-adrenergic receptor responsiveness. Hostility and satisfaction with perceived social support predicted ß-adrenergic receptor responsiveness in multiple linear regression analyses controlling for race, gender, age, SBP, and resting heart rate. High hostility was associated with reduced cardiac ß-adrenergic receptor function among both white and African American men. Low levels of satisfaction with social support were associated with reduced cardiac ß-adrenergic receptor responsiveness among men and women. Hostility and satisfaction with social support shared some variance in models predicting ß-adrenergic receptor responsiveness.

CONCLUSIONS: Reduced ß-adrenergic receptor responsiveness is associated with higher levels of hostility among men, and is associated with lower levels of satisfaction with social support among men and women. Impaired ß-adrenergic receptor function, which is a common characteristic of cardiovascular disease, may be a marker of increased cardiovascular disease risk among individuals high in hostility and low in social support.

Key Words: adrenergic receptor responsiveness, • Cook-Medley hostility, • social support.

Abbreviations: AR = adrenergic receptor;; BMI = body mass index;; CD25 = chronotropic dose of isoproterenol required to increase HR by 25 bpm;; DBP = diastolic blood pressure;; ECG = electrocardiogram;; Ho = Cook-Medley Hostility scale;; HR = heart rate;; MAP = mean arterial pressure;; PD25 = dose of phenylephrine required to increase MAP by 25 mmHg;; SBP = systolic blood pressure;; SSQ = Sarason Brief Social Support Questionnaire.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Individuals high in hostility are at increased risk for coronary heart disease and mortality (1–7), prompting numerous investigations of possible mechanisms, such as exaggerated sympathetic nervous system responses to stress (1, 8–10), low social support, and health damaging behaviors such as smoking, poor dietary habits, and medical nonadherence (1, 11). One feature of the sympathetic nervous system that has recently been related to hostility is cardiac beta adrenergic receptor (ß-AR) function. Reduced cardiac ß-AR responsiveness has been implicated in the pathophysiology of hypertension (12–17). Cardiac ß-AR responsiveness is impaired in ischemic heart disease (18, 19), and is strikingly compromised by congestive heart failure (20–22). Elevations in the kinase primarily responsible for ß-AR desensitization are evident early in the development of heart disease (23, 24), and some evidence suggests that reduced ß-AR responsiveness may be a preclinical marker of coronary heart disease (CHD) (25).

Two investigations have associated hostility with downregulation of ß-ARs. In one study, white men with higher Cook-Medley Hostility Scale (Ho) (26) scores were shown to exhibit altered mononuclear leukocyte ß-adrenergic physiology (27). This was reflected in reduced receptor density as well as reduced ß-AR responsiveness, which was expressed as greater forskolin-stimulated intracellular cyclic adenosine monophosphate generation. To the extent that mononuclear leukocyte ß-AR functioning is a valid model of cardiac ß-ARs (28), these results indicate that more hostile men may have downregulated cardiac ß-ARs. Similarly, a second study showed that white men with high Ho scores exhibit marginally reduced cardiac ß-AR responsiveness relative to those with lower Ho scores, based on their heart rate responses to an isoproterenol challenge (29). Higher Ho scores were also associated with reduced vascular ß2-AR responsiveness, as indicated by attenuated vasodilation responses to isoproterenol challenge. The effect of hostility on AR functioning was found to be specific to ß-ARs, because Ho scores were unrelated to {alpha}-AR responsiveness. Although preliminary, these combined findings suggest a relationship between hostility and ß-AR function and expression.

The primary purpose of the present study was to further document the relationship between hostility and ß-AR responsiveness and to extend this research to include women and minorities. In keeping with previous findings, we hypothesized that hostility would be related to reduced cardiac ß-AR responsiveness. We did not hypothesize that the magnitude or nature of this relationship would be different among women or African Americans. We did not expect hostility to be related to {alpha}-AR responsiveness.

A secondary purpose of the study was to examine the relationship between perceived social support and cardiac ß-AR responsiveness. Social support was selected for analyses involving AR responsiveness because of the centrality of social interactions and social support in theoretical models relating hostility to cardiovascular responses and cardiovascular risk (1, 30–32). In addition, low social support has been associated with higher plasma and urinary catecholamine levels (33–35), which could result in cardiac ß-AR downregulation. This is the first investigation of social support and ß-AR sensitivity, and we consider these analyses exploratory. Nevertheless, we hypothesized that individuals lower in social support would have reduced cardiac ß-AR responsiveness.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Participants
One hundred forty nine men and women aged 25 to 45 years (M = 33.2, SD = 5.8), who participated in the Biobehavioral Investigation of Hypertension study at Duke University Medical Center, are included in the current report. Duke University Medical Center’s Internal Review Board approved the study protocol, and all participants provided verbal and written consent before participation. There were 33 African American men, 38 African American women, 51 white men, and 27 white women. Individuals with SBP > 160 or DBP > 105 were excluded, as were individuals with a history of antihypertensive medication use. Mean SBP was 119.9 (SD = 13.3) and mean DBP was 78.9 (SD = 10.13). Resting HR averaged 65.4 (SD = 11.1), and mean BMI was 25.9 (SD = 3.4).

Psychosocial Measures
Hostility was assessed using Ho (26), a 50-item true/false questionnaire derived from the Minnesota Multiphasic Personality Inventory. The Ho scale measures cynical hostility with acceptable reliability and validity (36), is the most widely used self-report measure of hostility, and is prospectively related to coronary heart disease and angiographically determined severity of atherosclerosis (1).

Perceived social support satisfaction was assessed using the Brief Social Support Questionnaire (37). The Brief Social Support Questionnaire measures the number of perceived providers of social support for six common support scenarios, yielding a perceived availability score (SSQ Availability), as well as satisfaction with the perceived social support, yielding a satisfaction score (SSQ Satisfaction). On both scales, higher scores indicate greater levels of social support. Both scales for this measure have demonstrated internal consistency exceeding 0.9, adequate validity, and near equivalence with the full 27-item version of the Social Support Questionnaire (37, 38). In this sample, the correlation between SSQ Availability and SSQ Satisfaction scores was 0.29 (p < .01), and their correlations with Ho scores were -0.18 (p = .03) and -0.14 (p = .10), respectively.

Adrenergic Receptor Responsiveness Testing
All receptor responsiveness testing was conducted while participants were fully reclined in a sound attenuated, electrically shielded, temperature controlled room maintained at 74°F (23.3°C), and at least 6 hours after the most recent caffeine consumption. BP was measured continuously using the Finapres Model 2300 (Ohmeda, Madison, WI) noninvasive BP monitor, which uses the vascular unloading technique to measure SBP, DBP, and MAP on a beat-by-beat basis. This instrument has been validated against intra-arterial measures under various conditions, including pressor responses to phenylephrine (39). An ECG was recorded using disposable ECG electrodes in a lead II configuration and used to measure HR during AR responsiveness testing.

Resting BP and HR Measures
SBP and DBP were measured with the use of a BP monitor (model 4240, Suntech, Raleigh, NC), and HR was recorded from the ECG, during a 20-minute baseline rest period in the AR responsiveness testing room. Three measures taken during minutes 18–20 of the rest period were averaged to obtain resting HR, SBP, and DBP values.

ß-AR Responsiveness
The standardized isoproterenol sensitivity test was used to evaluate ß-AR responsiveness in terms of the chronotropic dose of isoproterenol required to increase HR by 25 bpm (CD25) (40). Progressively increasing bolus-doses of isoproterenol (0.125, 0.25, 0.5, 1.0, 2.0, and 4.0 µg) were injected into an antecubital vein until an increase in HR of at least 25 bpm was observed. HR responses after each dose were computed as the shortest three successive ECG R-R intervals after drug injection, compared with the shortest three R-R intervals at rest (preinjection). After each dose, the next higher dose was not injected for at least 5 minutes, or until cardiovascular activity had returned to resting levels, usually within 5-l0 minutes. The linear regression model of log-dose/HR response for each subject was used to determine CD25 exactly by interpolation. The CD25 measure provides an index of cardiac ß1 and ß2-AR responsiveness, and is inversely related to receptor responsiveness.

{alpha}1-AR Responsiveness
A procedure analogous to the ß-AR test described above was used for assessing {alpha}1 receptor responsiveness, using the {alpha} agonist phenylephrine to stimulate vascular {alpha}1 receptors (14). In this test, the criterion response is defined as the dose required to increase MAP by 25 mm Hg (PD25). An initial dose of 25 µg phenylephrine was used, with successive doses doubled until the 25 mm Hg response was exceeded, or until a maximum dose of 800 µg. Again, at least 5 minutes or longer if required for recovery of cardiovascular activity to resting levels, preceded administration of successive doses. The linear log-dose/MAP response curve was used to determine the exact PD25 dose. The PD25 index is inversely related to vascular {alpha}1 receptor responsiveness.

Analytical Strategy
All statistical analyses were performed using SAS software (SAS, Cary, NC). The criterion for statistical significance was set at p < .05. In preliminary analyses, race and gender categories were compared with respect to hostility and social support scores on using separate two (race) by two (gender) analyses of variance (ANOVA) tests. The primary analyses evaluating the relationship between Ho, SSQ availability, and SSQ satisfaction scores on {alpha}- and ß-AR responsiveness consisted of bivariate correlations and separate hierarchical multiple linear regression analyses. Because our previous research has documented independent and noninteractive effects of race, gender, and blood pressure on {alpha}- and ß-AR responsiveness, these variables were used as control variables. Categorical variables (ie, race and gender) were dummy coded, and interaction terms were not included. Age was used as an additional covariate in all regression equations, and resting HR was used as a covariate for analyses involving the CD25 index of ß-AR responsiveness. For all psychological variables found to predict {alpha}- and ß-AR responsiveness, interactions with race and gender were explored, and independent contributions of each psychological variable were evaluated.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Ethnic and Gender Comparisons for Hostility and Social Support Scores
African American participants had higher Ho scores (M = 21.8, SD = 7.4) than white participants (M = 18.8, SD = 6.0), F(1,145) = 5.3, p = .02, and lower SSQ Availability scores (M = 2.8, SD = 1.8) than white participants (M = 3.6, SD = 1.9), F(1,139) = 7.47, p = .01. Men and women had similar Ho and SSQ scores (p values > 0.28), and race and gender did not interact to predict hostility or social support scores (p values >0.30).

{alpha}-AR Responsiveness
There was a nonsignificant trend for Ho scores to be negatively related to the PD25 index of {alpha}-AR responsiveness (r = -0.15, p = .07), indicating a tendency for more hostile individuals to have greater {alpha}-AR responsiveness. Neither SSQ Satisfaction nor SSQ Availability scores were correlated with PD25 (r values < 0.06, p values > 0.48). Heirarchical multiple linear regression analyses were performed to evaluate the relationship between each psychological variable and 32 {alpha}-AR responsiveness (PD25) after controlling for appropriate covariates. The first step regressed PD25 on the linear combination of race, gender, resting SBP, and age. The equation containing these variables accounted for 21% of the variance in PD25 [F(4,142) = 9.21, p < .0001]. Significant beta weights were observed for race and gender (p values <0.05). In the second set of analyses, Ho, SSQ Availability, and SSQ Satisfaction were each added to the model in separate regression equations. None of these variables added significantly to the variance explained ({Delta}R2 values <0.01, F values <=0.74, p values >=0.39).

ß-AR Responsiveness
Ho scores were positively correlated with the CD25 index of ß-AR responsiveness (r = 0.25, p < .01), indicating that individuals high in hostility had reduced ß-AR responsiveness. SSQ Satisfaction scores were negatively correlated with CD25 (r = -0.22, p < .01), indicating that individuals reporting lower satisfaction with their social support had reduced ß-AR responsiveness. SSQ Availability scores showed a nonsignificant correlation with CD25 (r = -0.15, p = .08). Hierarchical multiple linear regression analyses were performed to further evaluate the relationship between each psychological variable and CD25. The first step regressed CD25 on the linear combination of race, gender, SBP, age, and resting HR. The equation containing these variables accounted for 17.9% of the variance in CD25 values [F(5,143) = 6.21, p < .001]. Significant beta weights were observed for gender and resting HR (p values < 0.05). In the second set of analyses, Ho, SSQ availability, and SSQ satisfaction scores were each added to the model in separate regression equations. When Ho scores were added to the model, an additional 3.9% of the variance in CD25 values was explained [{Delta}R2 = 0.04, F(1,142) = 7.10, p = .008]. When SSQ Satisfaction was added to the model, an additional 4.6% of the variance was explained [{Delta}R2 = 0.04, F(1,134) = 7.74, p = .006]. SSQ Availability scores did not contribute significantly to the variance explained in CD25 values [{Delta}R2 < 0.01, F(1,134) < 1, p = .34]. Table 1 presents regression statistics for Ho, SSQ Satisfaction, and SSQ Availability scores predicting CD25.


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  		TABLE 1. Heirarchical Multiple Linear Regression Analyses Predicting CD25 (µg)
 
Possible interactions of Ho and SSQ Satisfaction scores with race and gender were explored by adding appropriate interaction terms to the models generated in the second set of analyses. When the interaction of Ho scores and gender was added to the model, an additional 2.3% of the variance in CD25 values was explained [{Delta}R2 = 0.02, F(1,141) = 4.37, p = .04]. Hostility did not interact with race to predict CD25 values [{Delta}R2 < 0.01, F(1,141) < 1, p = .7]. SSQ Satisfaction scores did not interact with race or gender to predict CD25 values ({Delta}R2 values < 0.02, F values < 2.5, p values > 0.12).

To interpret the interaction of hostility and gender, multiple linear regression analyses were performed separately for each gender. CD25 was regressed on the linear combination of race, age, SBP, resting HR, and Ho scores for men and women separately. For men, the equation containing these variables accounted for 22% of the variance in CD25 [F(5,78) = 4.37, p = .002], and hostility was an independent predictor of CD25 (p = .01). For women, the equation containing these variables accounted for 23% of the variance in CD25 [F(4,60) = 5.59, p < .01]; however, hostility did not independently predict CD25 (p = .89).

The relative independent contributions of Ho and SSQ Satisfaction scores to the prediction of CD25 values were explored among men by adding relevant terms to a model that included race, age, SBP, and resting HR. Ho and SSQ satisfaction did not interact to predict CD25 (p = .57). Neither Ho (p = .11) nor SSQ Satisfaction (p = .08) remained independent predictors of CD25 when the other variable was entered first, suggesting that these constructs share some of their predictive power.

To illustrate the relationship between hostility and ß-AR responsiveness we observed among men, Figure 1 displays mean levels of the CD25 index of ß-AR responsiveness among men illustrated by tertiles of Ho scores. Tertiles of Ho scores were created separately for African American and white men, given the racial difference in Ho scores. The CD25 values for men in the highest tertile of Ho scores (M = 2.99, SE = 0.42) were roughly 85% higher than those of the men in the lowest tertile (M = 1.61, SE = 0.21), indicating significantly lower cardiac ß1 and ß2-AR responsiveness.



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  		Fig. 1. Values of CD25 for men in tertiles of hostility scores.

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
The study findings confirm previous observations that hostility, measured using the Ho Scale, is associated with blunted cardiac ß-AR responsiveness. More specifically, and in keeping with previous reports (27, 29), we found that more hostile men had reduced cardiac ß-AR responsiveness than men who were less hostile. Moreover, this was the first study to evaluate this relationship in African Americans, and we found that the relationship between hostility and ß-AR responsiveness was similar in both African American and white men.

Reduced ß-AR responsiveness associated with higher levels of hostility may reflect effects of chronic stress as well as larger catecholamine responses to stressful life events. Chronic stress has been associated with elevated plasma norepinephrine levels (41), and individuals high in hostility are thought to experience higher levels of chronic stress by virtue of their greater propensity for interpersonal conflict (1). In addition, individuals high in hostility have shown larger catecholamine responses during laboratory stressors (8, 42) as well as increased levels of urinary catecholamines (43). Frequent or sustained catecholamine elevations associated with hostility may, over a period of time, lead to down-regulation of cardiac ß-AR receptors.

This was the first study to extend an examination of hostility and cardiac ß-AR responsiveness to women. We did not find hostility to be related cardiac ß-AR responsiveness among women, as we had hypothesized. The women in this study were premenopausal, and had lower values of CD25 (M = 1.8, SD = 1.1) compared with the men in this study (M = 2.3, SD = 1.9), which is consistent with their lower relative risk of CHD. It is possible that including women with a larger range of CD25 values (eg, postmenopausal, higher BPs) would enhance our ability to detect significant associations of hostility and cardiac ß-AR responsiveness among women. Alternately, null findings for women may reflect gender differences in the experience and expression of anger and hostility (44), as well as gender differences in stress-evoked catecholamine responses thought to account for reduced cardiac ß-AR responsiveness (45).

This was the first study to explore possible associations of social support with {alpha}-and ß-AR responsiveness. We found that individuals reporting lower satisfaction with their perceived social support exhibited reduced cardiac ß-AR responsiveness. The perceived availability of social support was not significantly related to SSQ cardiac ß-AR responsiveness, although a trend was noted in the hypothesized direction (r = -0.14, p = .08). Satisfaction with social support and hostility appeared to share some variance in the prediction of cardiac ß-AR responsiveness among men, as the independent contribution of either variable was attenuated with the prior entry of the other.

These findings, though preliminary, are informative because social support is important in theoretical models relating hostility to cardiovascular responses and cardiovascular risk (1, 30–32). Higher levels of social support have been related to attenuated BP reactivity in the laboratory (46) as well as lower ambulatory BP levels (47). Interestingly, individuals high in hostility have greater cardiovascular responses primarily during interpersonal laboratory stress tasks (1, 9). Although more hostile individuals have been observed to have generally higher ambulatory BP (47), this may be particularly apparent during social interactions (48), may be partially accounted for by social stress (49), and may involve an interaction with social support (50). Therefore, we recommend that future research relating hostility and ß-AR responsiveness further evaluate the role of social support.

Limitations
Important limitations of this investigation must be noted. No data are available regarding the validity of the Sarason Brief Social Support Questionnaire (37) among African Americans, although we and other investigators (51) have used this measure in studies that have included African American participants. Another possible limitation is that our index of ß-AR responsiveness could have been affected by individual differences in baroreceptor reflexes, because it examines systemic effects of isoproterenol. However, isoproterenol infusion studies that do not involve the baroreflexes (52) have yielded similar results to our own previous data (15) for important comparisons such as race. In addition, hostility was associated with downregulation of ß-adrenergic receptor density on mononuclear leukocytes in previous research with white men (27). This study was also unable to evaluate causal relationships between ß-AR responsiveness and cardiovascular risk. For some diseases (eg, hypertension), downregulation of ß-AR related to hostility and low social support may exacerbate pathophysiology. Alternatively, ß-AR sensitivity may be a marker of cardiovascular disease risk, and may be related to hostility and social support by virtue of the cardiovascular risk associated with these psychosocial variables.


   CONCLUSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
ACKNOWLEDGMENTS
 REFERENCES
 
The results of this study add to the emerging evidence relating psychosocial variables to AR function. Our findings confirm that higher levels of hostility are associated with reduced cardiac ß-AR, but not {alpha}-AR responsiveness, among both white and African American men. We also found that low levels of satisfaction with social support are associated with reduced cardiac ß-AR responsiveness among African American and white men and women. Although the results are preliminary, it appears that hostility and satisfaction with social support share variance in predicting ß-AR responsiveness among men. Impaired AR receptor function, which is a common characteristic of cardiovascular disease (12), may be a marker of increased cardiovascular disease risk among individuals high in hostility and low in social support.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 ACKNOWLEDGMENTS
REFERENCES
 
This research was supported by National Institutes of Health Grants HL-49427 and M01-RR-30 General Clinical Research Centers Program, National Center for Research Resources.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 

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