Nocturnal sodium excretion, blood pressure dipping, and sodium sensitivity.

More than 30 years ago, Guyton1 described pressurenatriuresis: increasing arterial blood pressure promotes sodium excretion, decreasing blood volume and lowering blood pressure, whereas when blood pressure falls, sodium excretion decreases, and blood volume and blood pressure increase.1,2 The linchpin of the model of Guyton et al3 is the concept of feedback gain. Gain is the degree to which a feedback system can correct a perturbation, that is, the amount of correction of a deviation divided by the residual degree of deviation. When a control system corrects a perturbation minimally, its feedback gain is near 0. When it corrects it completely, its gain is infinite. As emphasized by Guyton et al,3 in integrated systems with infinite and finite gain components, the infinite gain function ultimately dominates. There are myriad blood pressure control systems, for example, arterial baroreceptors and chemoreceptors, the central nervous system ischemic response, the renin–angiotensin system, and capillary fluid shift, but all are ultimately trumped by pressure–natriuresis. In the experiments by Guyton et al,3 pressure-natriuresis had near infinite gain over a wide range of urinary sodium excretion, such that the set point of blood pressure regulation was not affected by sodium intake over a period of several days or a few weeks. This pressure–natriuresis model describes a steady-state relationship. At short time intervals, blood pressure and sodium excretion may not be closely linked, but the body will always eventually bring the system back into balance. In this review, we wish to draw attention to differences in the relationship of blood pressure to sodium excretion during day and night and to how nighttime pressure–natriuresis and sodium sensitivity of blood pressure interact. We will suggest that these features of pressure–natriuresis have implications both for the clinical management of hypertension and research into the genetic underpinnings of the disease.