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daytime blood pressure values ≤ 135/85 mmHg . Over the Expectedly, the prevalence of isolated nocturnal hypertensi-
7
past decade and a half, it has been demonstrated that de- on is lower and ranges from 6% among Western Europeans
viations from normal values in arterial blood pressure du- to 10.9% among residents of Japan .
12
ring the night (sleep) are associated with damage to target
organs, such as left ventricular myocardial hypertrophy,
“silent“ cerebral disease, and albuminuria, as well as sub- Mechanisms underlying the development
sequent atherosclerotic and cerebrovascular diseases. For of non-physiological changes in blood
all elevated blood pressure values during the night excee- pressure values during the night
ding 120/70 mmHg, we use the term nocturnal hyperten-
sion . In addition to the increase in mean nocturnal values, Physiological circadian variations in blood pressure are
8
with normal or elevated mean daytime values of blood influenced by changes in the activity of the autonomic ner-
pressure, nocturnal hypertension also includes distur- vous system (sympathetic and parasympathetic systems),
bances in the circadian rhythm, namely non-dipping and alterations in the levels of vasopressin, acetylcholine, adre-
nocorticotropic hormone, cortisol, insulin, ghrelin, adipo-
Image 1. Nocturnal hypertension nectin, and leptin, as well as the renin-angiotensin-aldo-
sterone system (RAAS). Fluctuations in the levels of these
hormones are responsible, under normal circumstances,
for higher blood pressure values during the day and lower
values during the night .
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There are numerous mechanisms responsible for
non-physiological changes in arterial blood pressure during
the night, such as increased activity of the sympathetic ner-
vous system, renin-angiotensin-aldosterone system, salt re-
tention, renal dysfunction, sleep apnea, and other sleep di-
sorders, obesity, aging, stress, and diabetes mellitus . All of
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these mechanisms contribute to increased blood pressure
during the day.
Dysregulation of the autonomic nervous system, with
reduced parasympathetic response during the night, is cha-
racteristic of the non-dipping pattern. On the other hand, it
has been found that there is decreased catecholamine ex-
cretion during the day compared to the nighttime period, as
well as increased sensitivity of alpha 1 receptors during the
Note: (includes an increase in AP ≥ 120/70 mmHg which can be isolated and with or
without the absence of expected nocturnal blood pressure dipping) night in patients with a non-dipper pattern.
reverse dipping patterns (Image 1). Since the extreme dip- Obstructive sleep apnea (OSA) is characterized by
ping pattern typically does not involve increased blood pre- frequent episodes of partial or complete collapse of the
ssure values, it will not be further discussed, and its impact upper airway during sleep. There is an association between
on cardiovascular risk is not fully elucidated. Palatini et al. sleep apnea and arterial hypertension (AH), cardiovascular
showed that this pattern did not lead to adverse outcomes diseases, and glucose metabolism disorders. OSA repre-
in individuals younger than 70 years old, but it was asso- sents a predisposing factor for the development of AH, and
ciated with a fourfold increase in the risk of cardiovascular conversely, there is a higher incidence of OSA in hyperten-
events in those older than 80 years old . sive patients. AH in patients with OSA is predominantly no-
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cturnal with a non-dipping pattern, with spikes in blood pre-
ssure during periods of apnea or hypopnea. In conditions of
Epidemiology of nocturnal hypertension apnea-induced intermittent hypoxia and sleep disruptions,
there is excessive sympathetic activity with consequent in-
Data on the prevalence of nocturnal hypertension are creases in arterial blood pressure .
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inconsistent because it varies depending on demographic,
clinical, and ethnic factors. The mentioned difference in A high salt intake, especially in salt-sensitive individuals,
defining nocturnal hypertension also contributes to these plays a significant role in the development of nocturnal ar-
14
variations. terial hypertension . It is also responsible for isolated no-
cturnal hypertension and for the non-dipping pattern, whi-
In the PAMELA study, nocturnal hypertension was found ch can be explained by the dominant excretion of excess salt
in 30% of participants, while in the study by Androulakis, during the night. It has been shown that nocturnal hyper-
which included patients with newly diagnosed arterial hy- tension is associated with low daytime and high nighttime
pertension, it was found in as many as 50% of patients 10, 11 . sodium excretion, and that restricting sodium intake leads
36 DOI: 10.5937/Galmed2409041I

