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Psychosomatic Medicine 66:289-290 (2004)
© 2004 American Psychosomatic Society

LETTERS TO THE EDITOR

HOSTILITY, CORONARY RISK, AND {alpha}-ADRENERGIC TO ß-ADRENERGIC RECEPTOR DENSITY RATIO

Jeffrey P. Kahn, MD

Weill Medical College, Cornell University, New York, New York

Hughes et al. (1) have published a wonderful study of the correlation between hostility and social support on the one hand, with in vivo {alpha}-adrenergic and ß-adrenergic receptor responsiveness on the other. One of the most interesting applications of these findings is to the spasm-injury theory of coronary artery atherogenesis. For example, {alpha}-receptor stimulation produces coronary vasoconstriction, while ß-receptor stimulation produces coronary vasodilatation. By that theory, chronic adrenergically mediated vasospastic activity should lead to a relative decrease in {alpha}-adrenergic receptor density, and to a relative increase in ß-adrenergic receptor density. Previous research has reported that measures of hostility and Type A behavior are associated in vitro with decreased {alpha}2-adrenergic receptor density on platelets, and with increased ß2-adrenergic receptor density on lymphocytes (2, 3). More importantly, the {alpha}2/ß2 receptor density ratio is a more refined physiological indicator model of recent vasoconstrictive activation, and is highly correlated with anger trait and Type A behavior in subjects with a family history of early coronary artery disease (2). It would be interesting to see the data by Hughes et al. (1) for a similar subgroup, and especially whether their in vivo data show a similar correlation of an {alpha}/ß-receptor responsiveness ratio with measures of hostility and social support.

REFERENCES

  1. Hughes JW, Sherwood A, Blumenthal JA, Suarez EC, Hinderliter AL. Hostility, social support, and adrenergic receptor responsiveness among African-American and white men and women. Psychsom Med 2003; 65: 582–7.[Abstract/Free Full Text]
  2. Kahn JP, Perumal AS, Gully RJ, Smith TM, Cooper TB, Klein DF. Correlation of Type A behaviour with adrenergic receptor density: implications for coronary artery disease pathogenesis. Lancet 1987; 8565: 1937–9,ii.
  3. Mills PJ, Shiller AD, Kuhn CM, Schanberg S, Williams RB, Zimmerman EA. The relationship between hostility and beta-adrenergic receptor physiology in healthy young males. Psychsom Med 1997; 59: 481–7.[Abstract/Free Full Text]

Response

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

Duke University Medical Center, Durham, North Carolina

We agree that one important implication of studies relating psychosocial characteristics to abnormal adrenergic receptor function is the potential impact on coronary vasomotor regulation. As might be expected from the independent relationships that we observed between hostility scores and our in vivo {alpha}1-adrenergic (r = -.15, p = .07) and ß-adrenergic (r = .25, p < .01) receptor responsiveness indices, the {alpha}1/ß ratio did indeed exhibit a significant negative correlation with hostility (r = -0.20, p < .05). We assessed family history of coronary heart disease (CHD) by asking subjects to indicate whether, to their knowledge, neither (N = 113), one (N = 34), or both (N = 2) parents had been diagnosed with CHD. Although family history of CHD was not found to moderate the relationship between hostility/social support and adrenergic receptor function, subjects with a positive family history (one or both parents) exhibited heightened {alpha}1-adrenergic receptor responsiveness compared with subjects with a negative family history (PD25: FH+ = 233 µg phenylephrine; FH- = 314 µg phenylephrine; p = .005 adjusted for gender, ethnicity, and blood pressure). In contrast, there were no differences associated with family history of CHD for ß-adrenergic receptor responsiveness (CD25: FH+ = 2.11 µg isoproterenol; FH- = 2.11 µg isoproterenol; p = .98), and the {alpha}1/ß ratio also was not significantly different (p = .1). These observations are consistent with the notion that downregulation of ß-adrenergic receptors associated with hostility may be of particular pathophysiologic significance in the context of {alpha}-adrenergic receptor hyperresponsiveness. Such an adrenergic receptor imbalance may favor {alpha}1-adrenergically mediated vasoconstriction, which in the coronary vessels has been associated with the potential to trigger myocardial ischemia (1). Interestingly, ß-adrenergically mediated vasodilation appears to be mediated in part via vascular endothelial nitric oxide release (2) and therefore is dependent on endothelial health, which is characteristically poor in patients with CHD. The relationship among hostility, social support, and ß-adrenergic receptor regulation that we observed suggests a plausible pathophysiologic pathway that may provide important insights into how these psychosocial traits may act as risk factors for CHD. However, the inability to establish cause-effect relationships remains a major limitation of the existing cross-sectional studies, and prospective studies are needed that would allow the natural history of the interrelationships between psychosocial characteristics, adrenergic receptor function, and the clinical manifestation of CHD to be more fully understood.

REFERENCES

  1. Dakak N, Quyyumi AA, Eisenhofer G, Goldstein DS, Cannon RO. Sympathetically mediated effects of mental stress on the cardiac microcirculation of patients with coronary artery disease. Am J Cardiol 1995; 76: 125–30.[CrossRef][Medline]
  2. Dawes M, Chowienczyk PJ, Ritter JM. Effects of inhibition of the L-arginine/nitric oxide pathway on vasodilation caused by beta-adrenergic agonists in human forearm. Circulation 1997; 95: 2293–7.[Abstract/Free Full Text]




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