| Biography: David E. Anderson received his Ph.D. in Clinical Psychology from the University of Oregon in 1966, and served a Postdoctoral Fellowship at the University of New York at Stony Brook, 1966-1967. His career interest in the behavioral origins of hypertension emerged while he was on the faculty at the Johns Hopkins University School of Medicine (1968-1981), where he developed an animal behavior model of hypertension. He elaborated this stress/salt interaction model while a Professor at the University of South Florida (1981-1987). He was a recipient of an NIH Research Career Development Award (1983-1987) and the Pavlovian Award for Biological Science in 1985. He joined the National Institute on Aging in 1987 as Chief of the Behavioral Medicine Section of the Laboratory of Behavioral Science, and became Chief of the Behavioral Hypertension Section, Laboratory of Cardiovascular Science in 1997. He joined the Clinical Research Branch, Translational Research and Medical Services Section in 2007. |
| Research Interests: Behavioral medicine research is concerned with the application of behavioral principles and methods to the study of the origins of, and interventions in, medical disorders. The role of behavioral science in cardiovascular research is to clarify the nature of the contingencies on behavior that participate in the development of cardiovascular disorders, and to develop behavioral interventions for their prevention or reversal. It is understood that such chronic disorders are multi-factorial in origin, involving genetic and possibly other environmental/behavioral factors, including especially diet. |
| The mediating mechanisms by which behavioral factors participate in hypertension and coronary artery disease remain to be clarified, but are also likely to be distinct from each other. While coronary artery disease is clearly linked with anger and hostility (and associated activation of the sympathetic nervous system), the extent to which this mechanism mediates the development of sodium-sensitive forms of hypertension is far from established. The preponderance of evidence suggests that the physiological concomitants of emotional inhibition can play a significant mediating role, especially in interaction with high dietary sodium intake. It is with investigations of the mechanisms by which behavioral factors contribute to the pathogenesis of sodium-sensitive hypertension that the work of this section is dedicated. |
| Stress, Salt and Blood Pressure: Previous research in this laboratory found that a combination of behavioral stress and high sodium intake resulted in experimental hypertension in large laboratory animals over periods of days. This form of hypertension was not prevented by adrenergic blockade or by renal denervation, but was accompanied by an inhibited breathing pattern that was conditioned to the experimental setting. Under these conditions, the inhibited breathing pattern increased pCO2 and transiently decreased plasma pH. The respiratory acidosis expanded plasma volume by a variety of pathways, including increased sodium/hydrogen exchange. One consequence was an increase in plasma concentrations of a circulating endogenous sodium pump inhibitor, termed marinobufagenin, a substance found in the skin of toads. This compound promotes natriuresis, but also increases vascular tone. Subsequent experimental studies with healthy human subjects showed that voluntary performance of breathing suppression using a biofeedback procedure was accompanied by comparable effects on renal sodium regulation as in the previous studies with laboratory animals. |
| More recent research in our laboratory found that high resting end tidal CO2 (PetCO2) is a risk factor for blood pressure sensitivity to high sodium intake, particularly in older humans. In addition, high resting PetCO2 was found to be an independent correlate of elevated resting systolic BP, especially in women who were low in trait anger. Thus, chronic hypoventilatory breathing pattern might be a risk factor for sodium sensitive forms of high blood pressure. We have also found that chronic stress is associated with slower breathing at rest than in others, especially women. Postmenopausal women were also found to have higher levels of an endogenous inhibitor of nitric acid that could contribute to their increased blood pressure sensitivity to high sodium intake. Taken together, these studies implicate daytime inhibited breathing pattern in long-term blood pressure regulation, and complement other findings that hypertension is potentiated by sleep apnea. |
| Ongoing Studies: A study is in progress to test the hypothesis that blood pressure sensitivity to high sodium intake in normotensive persons is a function of the inhibited breathing pattern and associated endogenous sodium pump inhibitors. Participants are placed on a low salt diet and a high salt diet for seven days each, during which ambulatory breathing pattern and blood pressure are monitored in the natural environment. In addition, blood and urine samples are collected systematically to determine the time course of changes in sodium balance and related hormones involved in blood pressure regulation. This study may provide a simple clinical test for sodium sensitivity and elucidate critical mechanisms mediating the role of behavior in the pathogenesis of chronic hypertension. |
Recent Publications:
- Anderson DE, Metter EJ, Hougaku H, Najjar SS. Suppressed anger is associated with increased carotid arterial stiffness in older adults. Am J Hypertens. 2006;19(11):1129-1134.
- Chesney MA, Darbes LA, Hoerster K, Taylor JM, Chambers DB, Anderson DE. Positive emotions: exploring the other hemisphere in behavioral medicine. Int J Behav Med. 2005;12(2):50-58.
|
