Decreased orthostatic adrenergic reactivity in non-dipping postural tachycardia syndrome.
Nocturnal blood pressure patterns are expressed as a consequence of both intrinsic circadian rhythms and the quantity and quality of sleep. A range of neurohumoral factors have been either inferred or definitively proven to influence the circadian blood pressure pattern. In this regard, changes in atrial natriuretic peptide, plasma renin activity and plasma aldosterone have been evaluated as to the influence each might have in determining diurnal blood pressure patterns. As an example, a clear pattern of nocturnal increase in plasma renin activity has been observed; however, the relationship between this change and nocturnal blood pressure remains vague. In contrast, change in sympathetic nervous system activity has most commonly been associated with the conversion of a pattern of nocturnal dips in blood pressure to one of non-dipping. Increasingly, dietary intake patterns, characterized by high sodium or low potassium content, or both, are recognized as modifiers of the normal decrease in nocturnal blood pressure, again in favor of producing a non-dipping pattern. The impact of these nutritional patterns on nocturnal blood pressure change is recognized to be most prominent in salt-sensitive individuals. Modifications of dietary sodium intake, such that it is decreased or potassium intake is increased, or both, are now recognized as means by which a nocturnal non-dipping pattern can be converted to a dipping pattern. Additional studies of an integrative nature will be necessary to obtain more complete definition of the dynamic interplay between nutrition and various neurohumoral axes in determining how nocturnal blood pressure patterns are expressed.