Hypertension is a major risk factor for cardiovascular disease, which is a serious health problem in the highly industrialized countries. In more than 95% of the cases, the etiology of hypertension remains unknown. A key role in the etiology of hypertension is played by endothelial dysfunction and the inflammatory reaction in the vascular wall, in which the low molecular weight proteins so called chemokines are involved. The chemokines involved in the pathogenesis of hypertension include monocyte chemoattractant protein-1, MCP-1, CCL2, interferon-inducible protein (IP-10; CXCL10), interleukin-8 (IL-8; CXCL8), RANTES (CCL5), fractalkine (CX3CL1) and their receptors CCR2, CCR5, CXCR1, CXCR2, CXCR3 and CX3CR1. The mechanisms involving chemokines and their receptors in the pathogenesis of hypertension are complex and not fully understood. They include the impact of the migration of macrophages and monocytes to the vascular wall, endothelial dysfunction, effects on nitric oxide and endothelin-1 and smooth muscle cell proliferation. Chemokines are also involved in the pathogenesis of complications of hypertension, such as atherosclerosis, myocardial and renal fibrosis. In Poland, only about 26% of patients are effectively treated with antihypertensive drugs. The use of new therapeutic methods based on the inhibition of the inflammatory process in the vascular wall, including the impact on the function of chemokines and their receptors, could improve the effectiveness of the treatment of hypertension.

Obstructive sleep apnea (OSA) and arterial hypertension (AH) are closely linked disorders with common pathophysiological features. The present study aimed to investigate the relationship between AH and OSA by examining sleep architecture, vitamin D concentration and electrolyte levels in patients with these coexisting conditions. A total of 133 patients suspected of having OSA were recruited for examination. The participants were divided into 2 groups: hypertensives (n = 52); and normotensives (n = 81). One full-night polysomnographic examinations were conducted, followed by the statistical analysis of the collected data. Hypertensive individuals displayed increased apnea-hypopnea index (AHI), oxygen desaturation index (ODI), respiratory arousal index (RAI), and periodic limb movement index (PLMI) as compared to non-hypertensive individuals. Moreover, sleep efficiency (SE), the bruxism arousal index (BAI) and oxygen saturation (SpO2) level were decreased in the hypertensive group. In terms of biochemical parameters, hypertensive individuals exhibited a lower magnesium (Mg) level, and higher levels of C-reactive protein (CRP), uric acid (UA) and glucose. Notably, there were no statistical differences in vitamin D concentration between hypertensive and normotensive individuals. The study explored the potential influence of calcium (Ca), Mg, vitamin D, and UA concentrations on the sleep architecture of patients with comorbid AH and OSA. The findings revealed several notable associations. Firstly, sleep fragmentation correlated with Ca level, suggesting a potential role for both Ca and vitamin D in sleep arousals. Secondly, a higher UA concentration was linked to a higher AHI and increased sleep fragmentation. Additionally, alterations in Mg concentration were observed among hypertensive individuals with OSA. However, further research is needed to fully comprehend the potential impact of these factors on the sleep architecture of hypertensive individuals with apnea.

Hypertension is the most common risk factor for stroke, coronary heart disease and heart failure, which are the leading causes of death worldwide. Dietary patterns and supplements intakes are becoming important factors in the hypertension. The aim of this study was to estimate the effects of new generation egg yolk phospholipids rich in lecithin (SL) esterified with omega-3 and omega-6 fatty acids on blood pressure in hypertensive rats (SHR). Here we have reported that lecithin (SL) derived from egg yolk lowers blood pressure in pathology of hypertension. The SHR rats treated with SL had significantly lower blood pressure than control group (157/104 vs. 178/121 mmHg; P < 0.05) and down-regulated mesenteric artery over-response to norepinephrine and potassium chloride, giving similar arterial response as for normotensive Wistar Kyoto rats (WKY). Hypertensive rats treated by SL demonstrated significantly lower serum level of inflammatory factors. This work also indicates that SL treatment lowers heart rate and reduces the serum level of oxidative stress marker - nitrotyrosine - by 30–34% in both hypertensive and normotensive animals. Phospholipids with lecithin derived from PUFA fortified eggs may be a valuable dietary supplement in prophylaxis of hypertension and in patients with hypertension, however, this requires further studies on humans.

Background: Sleep bruxism (SB) is a common sleep-related movement behavior with a complex etiology. A recent hypothesis suggests psychoactive substance usage, tobacco smoking, and alcohol intake are risk factors for SB. This study aimed to evaluate SB intensity in tobacco smokers and alcohol drinkers. Methods: A total of 133 adults underwent full-night audio- and video-polysomnography, and the polysomnograms were evaluated using the American Academy of Sleep Medicine guidelines. The study group was divided into smoker and nonsmoker groups as well as drinker and non-drinker groups. Results: The results of the polysomnographic analysis confirmed that tobacco smoking has a significant effects on SB. Tobacco smokers showed increased bruxism intensity (5.50 ± 4.71 vs. 3.83 ± 3.26, p < 0.05), especially the mixed phenotype (0.93 ± 1.00 vs. 0.59 ± 0.59, p < 0.05), in the N1 sleep stage (22.84 ± 20.45 vs. 15.66 ± 13.60, p < 0.05) and the nonsupine position (4.93 ± 5.56 vs. 2.50 ± 2.31, p < 0.05). They also showed a higher number of bruxism episodes with arousal compared with nonsmokers (2.91 ± 2.83 vs. 1.61 ± 1.49, p < 0.05), indicating increased sleep fragmentation. However, no significant effect of alcohol on SB intensity was observed, and the bruxism episode index was similar in alcohol drinkers and nondrinkers. In addition, electrolyte disturbances and lipid disorders were evaluated. Compared with nonsmokers, tobacco smokers showed a higher concentration of plasma triglycerides (177.67 ± 106.9 vs. 129.18 ± 65.61) and lower levels of iron and magnesium (96.68 ± 43.58 vs. 123.83 ± 52.36 and 1.85 ± 0.22 vs. 1.96 ± 0.21, respectively). Conclusions: In summary, this study showed that tobacco smoking, but not alcohol consumption, is related to bruxism intensity and lipid and electrolyte disturbances in individuals with sleep disorders.

Sleep bruxism (SB) is a common behavior that can result in various clinical consequences on human health. Risk factors for SB include among others emotional stress, anxiety, tobacco smoking, and excessive alcohol consumption. Coffee and black tea are among the most commonly consumed beverages worldwide. This study explores the influence of coffee and black tea consumption on bruxism intensity, as observed in polysomnographic examination. Polysomnographic examination with simultaneous camera recording was conducted in 106 adult subjects. The results were evaluated according to guidelines set out by the American Academy of Sleep Medicine (AASM). The study group was divided according to habitual stimulant usage, as declared by the participants in a self-reported questionnaire. Four groups were identified: coffee drinkers versus non-drinkers and black tea drinkers versus non-drinkers. The bruxism episode index (BEI) was increased in coffee-drinkers as opposed to non-drinkers (4.59 ± 3.44 vs. 2.87 ± 1.50, p = 0.011). Sleep fragmentation, measured according to the arousal index, was comparable in coffee drinkers and non-drinkers. Electrolyte and lipid levels were similar in coffee drinkers and non-drinkers. Habitual black tea intake did not affect sleep architecture or bruxism intensity. The study showed that habitual coffee consumption is a risk factor for the increased intensity of sleep bruxism. Neither coffee nor tea consumption is related to sleep fragmentation in habitual drinkers. Coffee and tea intake does not affect electrolyte and lipid concentrations. Caution should therefore be recommended in drinking coffee in people with sleep bruxism.

Introduction: Comorbid insomnia and obstructive sleep apnea (COMISA) is not a well-identified sleep disorder, despite having a significant impact on health. This study investigates the relationship between sleep bruxism (SB) and sleep architecture in patients with COMISA, obstructive sleep apnea (OSA), and in those without any sleep disorders. Methods: 119 patients were included in the study and divided into three groups: OSA, COMISA, and a control group. Polysomnographic (PSG) examination provided parameters related to sleep architecture, OSA, and characteristics of SB. Results: The bruxism episode index (BEI) and other SB parameters were not found to be statistically different between the three groups (p > 0.05). There was no statistical difference in measured sleep architecture between the COMISA and OSA groups (p > 0.05). In comparison to the control group, participants in the COMISA group were found to have an increased apnea–hypopnea index (AHI), oxygen desaturation index (ODI), respiratory disturbance index (RDI), all arousals (AA), and respiratory arousals (RA) (p < 0.05). Among COMISA patients, AA and RA were shown to have a positive linear correlation with the number of bradycardia events per hour (r = 0.49, r = 0.48, p < 0.05). Conclusions: SB does not occur in patients with COMISA more frequently than in patients with OSA or those without any sleep disorders. PSG parameters are not specific for COMISA; therefore, in order to differentiate this disorder from OSA alone, a comprehensive patient assessment has to be performed.