No abstract

The interpretation of plasma norepinephrine (NE) levels is not straightforward because such levels represent a complex of synaptic discharge, metabolism, uptake, and regional blood flow. Some investigators have argued that peripheral NE levels bear little semblance to sympathetic nervous system activity affecting the cardiovascular system. This study examines this question in further detail. Eleven men (average age = 29) were studied. Plasma NE levels were obtained through continuous blood withdrawal from an antecubital vein, and simultaneous blood pressures were also monitored. Each subject was studied during four 4-min intervals of rest and during four 4-min intervals of a psychiatric stress interview. The interview was a friendly, intense discussion about upsetting situations the subject faced. The interview was a powerful and consistent tool for evoking physiologic responses. It led to an 83% increase in NE levels across all time intervals (p less than 0.001). During these same intervals, systolic pressure increased by 16 mm (p less than 0.0003) and diastolic by 13 mm (p less than 0.0001); furthermore, systolic and diastolic pressures were correlated with peripheral NE levels. This implies that the increased peripheral NE level was not merely a local phenomenon but reflected a signal affecting the entire vascular system.

Most research on reactivity to stressors limits its focus to the neurohormonal and cardiovascular components of reactivity. There is, however, another area of investigation with important implications to this field. Receptor binding techniques provide a direct measure of the functional link between neurohormonal signals and the responses they stimulate. Receptor measurement would enable psychophysiologic studies to begin to address the complete triad of signal emission/reception/end-organ response that underlies all reactivity patterns. This paper reviews adrenergic receptor physiology, methods, and research pertinent to reactivity. Our intention is to encourage greater consideration of these important issues in reactivity research.

Numerous physiological and biochemical factors contribute to the dynamic regulation of the cardiovascular system. This study used a cluster analytic statistical technique to discern patterns of adrenergic receptors and adrenergic agonists underlying cardiovascular responses to a laboratory challenge. Fifty hypertensive and normotensive black and white individuals had their beta- and alpha-adrenergic receptor sensitivity determined through agonist infusions. Norepinephrine, epinephrine, blood pressure, and heart rate responses to a standardized mental arithmetic task were also obtained. The cluster analysis identified four subgroups of individuals having distinct patterns of receptor and neurohormonal regulation of end-organ responses. In general, the data indicated that end-organ cardiovascular responses are, in part determined by the sensitivity of adrenergic receptors and the accompanying catecholamine responses. The findings also suggest that for some individuals nonadrenergic factors play a more dominant role than adrenergic mechanisms in determining cardiovascular pressor responses.

We examined the ability of baseline measures of receptors (lymphocyte beta-adrenergic) and nonreceptors (plasma catecholamines, heart rate, and blood pressure) to predict cardiovascular responses to a mental arithmetic task. Twenty-five male volunteers served as subjects. Nonreceptor measures predicted the heart rate response to stress poorly (p = 0.67). However, beta receptor density and sensitivity explained 48.4% of the variance in heart rate response (p = 0.007). When both receptor and nonreceptor measures were used together, they predicted 76.6% of the variance (p = 0.005), which was more than was explained by either receptor or nonreceptor baseline measurements alone (p = 0.001). Receptor measures may thus greatly improve the prediction of reactivity.