A technology-enabled service for perinatal collaborative care models: A randomized clinical trial.

Blood pressure (BP) exhibits pronounced circadian variation under normal physiological conditions, characterized by higher pressures during the daytime active period and a nocturnal decline during sleep. In healthy individuals, nighttime BP typically decreases by approximately 10–20% relative to daytime values, a pattern commonly referred to as the “dipper” phenotype [–]. In contrast, attenuation or absence of the normal nocturnal BP reduction, termed “non-dipping,” is strongly associated with adverse cardiovascular and renal outcomes, including left ventricular hypertrophy, stroke, chronic kidney disease progression, and increased mortality [,]. Non-dipping phenotypes are particularly prevalent in salt-sensitive hypertension, chronic kidney disease, diabetes, obesity, aging, and sleep disorders, suggesting that abnormalities in circadian BP regulation may represent an important component of cardiovascular and renal pathophysiology []. Despite extensive clinical and experimental investigation, the physiological mechanisms responsible for the emergence of non-dipping behavior remain incompletely understood. Multiple interacting systems contribute to circadian BP regulation, including the autonomic nervous system, vascular tone, sleep-wake transitions, hormonal regulation, renal sodium handling, and intrinsic molecular circadian clocks [,]. Experimental studies have demonstrated circadian oscillations in renal transporter expression and activity, glomerular filtration, renin-angiotensin-aldosterone signaling, sympathetic activity, and vascular reactivity [,]. At the same time, behavioral sleep-state transitions independently alter sympathetic drive, vascular resistance, and sodium handling []. Because these systems interact nonlinearly across multiple physiological timescales, isolating their individual and collective contributions to BP dipping experimentally is challenging. Renal sodium handling is believed to play a particularly important role in the pathogenesis of non-dipping hypertension. Experimental and clinical studies have linked impaired daytime sodium excretion with nocturnal hypertension and enhanced nighttime natriuresis, suggesting that elevated nighttime BP may partially compensate for inadequate sodium excretion during the active period [,]. More broadly, kidney-centered interpretations of non-dipping have proposed that abnormalities in pressure natriuresis and sodium balance may represent central physiological drivers of altered circadian BP regulation []. However, the extent to which circadian renal transport rhythms, behavioral sleep-wake modulation, and vascular rhythmicity independently contribute to physiological dipping and coordinated natriuresis remains unclear.