Abstract
The morning surge in blood pressure (BP) coincides with increased cardiovascular (CV) events. This strongly suggests that an altered circadian rhythm of BP plays a crucial role in the development of CV disease (CVD). A disrupted circadian rhythm of BP, such as the non-dipping type of hypertension (i.e., absence of nocturnal BP decline), is frequently observed in metabolic disorders and chronic kidney disease (CKD). The circadian timing system, controlled by the central clock in the suprachiasmatic nucleus of the hypothalamus and/or by peripheral clocks in the heart, vasculature, and kidneys, modulates the 24 h oscillation of BP. However, little information is available regarding the molecular and cellular mechanisms of an altered circadian timing system-mediated disrupted dipping pattern of BP in metabolic disorders and CKD that can lead to the development of CV events. A more thorough understanding of this pathogenesis could provide novel therapeutic strategies for the management of CVD. This short review will address our and others’ recent findings on the molecular mechanisms that may affect the dipping pattern of BP in metabolic dysfunction and kidney disease and its association with CV disorders.
Highlights
Blood pressure (BP) usually follows a circadian pattern of oscillation over a 24 h period with a decline of 10–20% at nighttime, and this normal pattern is referred to as the dipping pattern of BP [1]
A more thorough understanding of how the circadian timing system is related to the non-dipping pattern of BP in metabolic dysfunction and chronic kidney disease (CKD) would be helpful in developing novel therapeutic strategies for preventing the onset and development of CV disease (CVD)
All of these findings suggest that the molecular components of the circadian timing system are involved in the development of tubulointerstitial fibrosis, which in turn is linked to the development of an abnormal circadian rhythm of BP in CKD
Summary
Blood pressure (BP) usually follows a circadian pattern of oscillation over a 24 h period with a decline of 10–20% at nighttime, and this normal pattern is referred to as the dipping pattern of BP [1]. The loss of this nocturnal decline, i.e., the development of a non-dipping type of BP, is frequently observed in metabolic disorders and chronic kidney disease (CKD) and contributes to the development of cardiovascular (CV) disease (CVD) [2]. In this review, we summarize the recent findings on the molecular mechanisms related to the involvement of an altered circadian timing system in the development of the non-dipping pattern of BP and subsequent CVD in subjects with metabolic dysfunction and CKD. We discuss currently available and possible future chronotherapeutics that may be useful for patients with metabolic disorders and kidney disease
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