Nocturnal hyperarousal state in hypertension

In various pathological conditions (hypertension, sleep apnea, multinfarctual encephalopathy, etc.), the circadian pattern of blood pressure (bp) is flattened due to the absence or reduction of the physiological fall during sleep (non-dipping). Up to now, the neurophysiological meaning of this alteration is not completely known. In previous works [1, 2] we studied the prevalence of non-dipping phenomenon in two groups of patients (recently untreated young hypertensive and normotensive subjects with a family history of hypertension).We made a noninvasive, online recording of beat-to-beat bp values (Finapres 2300) with polysomnography (statistical analysis of mean bp profiles versus macro- and microstructure of sleep) for the assessment of the "autonomic cardiovascular drive" in basal and reproducible circumstances. The nocturnal reduction rate, an index expressing the bp fall during sleep state (NRR % = wake bp - slow wave sleep bp × 100/ wake bp) was calculated for systolic and diastolic values. By this methodological approach we showed that the same sleep microstructural aspects (increased number of microarousals) [3], were present in both groups (hypertensive and normotensive) of patients exibiting the non-dipper profile. We suggest for those patients, at the level of the multioscillatory systems regulating sleep mechanisms (brainstem and corticothalamic loops), the presence of a "neurogenic instability" lowering the threshold of production of endogenous microarousals. This "primary nocturnal hyperarousal state," probably genetically transmitted, acts as priming factor of a cascade of pathological events leading to and maintaining in this peculiar group of patients the hypertensive state.