Abstract
In human plasma, the concentration of free dopamine (DA) is approximately equal to that of epinephrine (E). Like norepinephrine (NE) and E its concentration may increase during physical effort and stress (Fig. 1). Most of the stress-related increase in plasma DA is derived from peripheral noradrenergic nerve terminals and the adrenal medulla. Because virtually all of the DA is rapidly conjugated upon release, it is necessary to measure plasma total (free + conjugated) DA. When dietary sources are controlled, the total DA concentration can be used as an indicator of the intensity of the sympathetic response and possibly the level of training in animals and humans. In normal individuals, plasma DA and blood pressure (BP) are usually negatively correlated since during a low level sympathetic discharge the hypotensive action of DA via dopaminergic vascular receptors predominates. The DA action on BP is, however, biphasic and dependent on its concentration. In many hypertensive patients, hypertensive peaks, which cannot be accounted for by rises in NE and E, are associated with very large stimulus-elicited increases in total DA into a range in which its hypertensive action via beta and alpha-receptors could temporarily predominate. Alternatively, this rise in DA could be a marker of the sympathetic discharge or a negative modulator of other hypertensive influences rather than the cause of the elevated BP. In primary aldosteronism, there is a more sustained increase in circulating DA. In both groups of patients the DA levels decrease with successful treatment. Concentrations of total DA and of free + conjugated NE + E in plasma are a more sensitive measure of sympathetic activity than are levels of free catecholamines, and they may provide a clinically useful biochemical index for categorizing hypertension and following its treatment.
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