Dipper and Non-Dipper Blood Pressure 24-Hour Patterns: Circadian Rhythm–Dependent Physiologic and Pathophysiologic Mechanisms

Abstract

Neuroendocrine mechanisms are major determinants of the normal 24-h blood pressure (BP) pattern. At the central level, integration of the major driving factors of this temporal variability is mediated by circadian rhythms of monoaminergic systems in conjunction with those of the hypothalamic-pituitary-adrenal, hypothalamic-pituitary-thyroid, opioid, renin-angiotensin-aldosterone, plus endothelial systems and specific vasoactive peptides. Humoral secretions are typically episodic, coupled either to sleep and/or the circadian endogenous (suprachiasmatic nucleus) central pacemaker clock, but exhibiting also weekly, monthly, seasonal, and annual periodicities. Sleep induction and arousal are influenced also by many hormones and chemical substances that exhibit 24-h variation, e.g., arginine vasopressin, vasoactive intestinal peptide, melatonin, somatotropin, insulin, steroids, serotonin, corticotropin-releasing factor, adrenocorticotropic hormone, thyrotropin-releasing hormone, endogenous opioids, and prostaglandin E2, all with established effects on the cardiovascular system. As a consequence, physical, mental, and pathologic stimuli that activate or inhibit neuroendocrine effectors of biological rhythmicity may also interfere with, or modify, the temporal BP structure. Moreover, immediate adjustment to exogenous components/environment demands by BP rhythms is modulated by the circadian-time-dependent responsiveness of biological oscillators and their neuroendocrine effectors. This knowledge contributes to a better understanding of the pathophysiology of abnormalities of the 24-h BP pattern and level and their correction through circadian rhythm-based chronotherapeutic strategies.

Sleep-time BP: prognostic marker of type 2 diabetes and therapeutic target for prevention

“…Accordingly, blocking the renin-angiotensin-aldosterone system by bedtime treatment seems to be an efficient means of reducing the asleep BP mean and increasing the sleep-time relative BP decline towards the normal dipper pattern. Despite the multiple factors influencing the mostly predictable daily BP variation and sleep-BP level, including rest-activity associated changes in behaviour, day-night cycles of environmental phenomena, and innate circadian (~24 h) rhythms in neuroendocrine, endothelial and haemodynamic variables [1,43,44], the impact of hypertension treatment-time on asleep BP regulation might thus be clinically relevant not only for CVD risk reduction-as previously documented [20][21][22], but also for preventing new-onset diabetes [32].…”

The Complex Relationship Between CKD and Ambulatory Blood Pressure Patterns

“…33 However, the final common pathway in the circadian rhythm of BP appears to be the symphathetic nervous system. Multiple investigations have shown the importance of the sympathetic nervous system including alpha-adrenergic regulation for the circadian change of vascular tone 34 , circadian variation in levels of both norepinephrine and epinephrine mirroring the change in BP, 35 and muscle sympathetic nerve activity correlating with nocturnal dipping of BP.…”

Non-dipping nocturnal blood pressure and psychosis parameters in Parkinson disease

“…[7] Twenty-four hour patterns and any associated circadian dysrhythmia, particularly an impaired blood pressure rhythm, have recently become of great interest to clinicians [8]. A blunted or even a reversed blood pressure circadian rhythm (e.g.…”