Ambulatory blood pressure monitoring provides information about the day-night blood pressure profile, which can be divided into dipping and non-dipping pattern. Non-dipping hypertension is recently thought to have increased cardiovascular risk and outcomes than dipping hypertension. The dipping pattern is explained by physiological changes in circadian rhythm, while the pathomechanism of non-dipping hypertension is not fully understood. Is it considered to be a result of many factors, such as: sympathetic nervous system overactivation, which can be accompanied by impaired parasympathetic nervous system response, obesity, concurrent diabetes mellitus and metabolic syndrome. Moreover abnormalities of hormones levels such as melatonin, catecholamines, thyroid and parathyroid hormones are connected to occurrence of non-dipping hypertension. Other widely discussed problem is obstructive sleep apnoea and its influence on circadian rhythm changes. Also dysfunction in activity of renin-angiotensin-aldosterone axis is thought to cause non-dipping pattern. There are some studies that indicate on role of inappropriate sodium intake in mentioned pathology. The chronic kidney disease and relationship with non-dipping hypertension will be also described. The last considered factor is influence of age on the development of non-dipping hypertension. key words: circadian blood pressure profile, blood pressure regulation, chronobiology, nocturnal hypertension, non-dipping pathomechanism

Due to high prevalence of hypertension (HT) in worldwide population, all aspects of this disease are studied in order to understand its pathogenesis and the influence on human body, as well as in order to find proper treatment. Impaired balance of autonomic nervous system (ANS) is taken into account as one of the main causes elevating blood pressure (BP). It seems that over-activation of sympathetic nervous system (SNS) is the most important factor in pathogenesis of HT. There are some methods which allow us to measure the sympathetic and parasympathetic nervous system activity. Some of them are described below and the influence of impaired ANS balance on HT development is presented. Many different, natural and pathologic factors can cause SNS response, so the measurement of the sole ANS activity cannot fully answer the question about the pathomechanism underlying HT. In this paper, we present some hypotheses regarding possible mechanisms of the disease progression. In primary HT, impairment of baroreceptors response is considered one of such mechanisms. Another one is the influence of hyperinsulinemia on the activation of SNS in insulin resistant patients. A few other factors are considered, like obesity, salt intake, sodium retention and alcohol intake and they are described briefly in our paper. In secondary hypertension, SNS can be activated indirectly by comorbidities, and this pathomechanism is also discussed.

Background. Non-dipping hypertension might be associated with increased cardiovascular risk and multiple diseases. The aim of our study was to assess if there are parameters identified in 24-hour ECG-Holter monitoring (ECG-Holter), transthoracic echocardiography (TTE), ECG parameters or laboratory data that allow prediction of circadian blood pressure profile (CBPP). Material and methods. One hundred and three consecutive patients (male: 50.5%), who underwent 24-hour ambulatory BP measurement and ECG-Holter simultaneously were analyzed. We divided patients into 3 groups: dipping was defined as 10-20% (28.2%), non-dipping as < 10% (50.5%) fall in nocturnal BP and reverse-dipping as higher nocturnal than diurnal BP (21.4%). Additionally, we performed TTE and laboratory check-up in all patients. We built multivariable models for nocturnal fall in systolic BP (SBP) and CBPP. Results. Multivariable model based on clinical factors was: nocturnal fall in SBP (%) = [13.28 -0.11 × age -8.33 × (dilated cardiomyopathy) -5.95 × PAD -6.02 × a-adrenolytic]. Multivariable model based on laboratory, echocardiographic and electrocardiographic parameters was: nocturnal fall in SBP (%) = [-27.28 + 1.47 × hemoglobin -0.14 × CK-MB + 0.14 × maximal heart rate]. Multivariable model for CBPP based on clinical factors included use of bor a-adrenolytics or torasemide.Conclusions. We proved that nocturnal fall in SBP and CBPP could be predicted based on ECG-Holter parameters, laboratory data and TTE results, as well as based on detailed medical history. These findings may have implications on care of patients with hypertension.