Determinants of Nondipping in Nocturnal Blood Pressure and Specific Nonpharmacological Treatments for Nocturnal Hypertension

N ondipper, diminished nocturnal blood pressure (BP) is an important predictor of hypertensive target organ damage and cardiovascular events. Various mechanisms have been reported so far to explain the nondipper phenomenon. Physiologically, an increased parasympathetic activation and a decreased sympathetic activation during sleep lead to a tendency for the nocturnal BP to decrease. In pathological conditions, such as sleep apnea syndrome, the sympathetic activation provoked by frequent arousal has been reported to be associated with the nondipper phenomenon.1,2 Matthews et al. used the fragmentation index, as evaluated by actigraphy to assess sleep quality, and found an increase in this index to be associated with a diminished nocturnal BP fall.3 In addition, more direct measurements of sleep quality derived from polysomnography also demonstrated both the macro (the greater the proportion in Stage 1 sleep and the smaller the proportion in rapid eye movement sleep )and micro (the greater the number of arousals)-sleep architectures to be associated closely with a dipping status in nocturnal BP, thus indicating a close association between poor sleep quality and nondipping. On the other hand, a higher nocturnal BP and the nondipper phenomenon are closely associated with a greater sodium intake. Some studies have reported the nondipper phenomenon to be associated with a reduced excretion of sodium during the daytime.4,5 The increase in BP observed during the night is a pressure-natriuretic mechanism favoring a compensatory rise in sodium excretion and the maintenance of sodium balance.5 An impaired renal capacity to excrete sodium into urine is an important mechanism of nocturnal hypertension in African-American hypertensives.6 Unfortunately, Matthews et al. did not investigate this mechanism. That study population consisted of 40% African Americans, and therefore sodium excretion and the maintenance of sodium balance might be an important mechanism of nocturnal hypertension. On the basis of the two major pathophysiologies of nondipper discussed earlier, an improvement in the sleep quality and a reduced salt intake with increased urinary sodium excretion would therefore be practical specific nonpharmacological treatments for nocturnal hypertension. The efficacy of these treatments would, however, differ among individuals with different mechanisms inducing the nondipper phenomenon.