The present research aimed to investigate the influence of sleep bruxism (SB) intensity on blood pressure parameters in normotensive subjects by using an ambulatory blood pressure device. The study group included 65 normotensive individuals suspected of having SB. All participants underwent one-night video-polysomnography, and ambulatory blood pressure monitoring was performed the next day; 86.15% of them were diagnosed with SB. Statistical analysis included correlation and regression analysis. The obtained results showed that systolic blood pressure variability during sleep significantly increased in individuals with BEI > 4 (bruxism episodes index; episodes/hour) compared to those with BEI ≤ 4 (8.81 ± 3.36 versus 10.57 ± 3.39, p = 0.05). Multivariable regression analysis showed that systolic blood pressure variability at nighttime was also associated with the following independent risk factors: higher apnea-to-bruxism index, male gender, BEI > 4 episodes/hour, body mass index (BMI) ≥ 25 kg/m2, higher arousal index, and shorter total sleep time. In summary, sleep bruxism intensity was associated with increased systolic blood pressure variability during sleep. Coincidental apnea, male gender, severe sleep bruxism (SB intensity with BEI > 4/hour), excess weight and obesity, higher arousal index, and shorter sleep time seem to be the main determinants that influence blood pressure in normotensive sleep bruxers.

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Primary hyperaldosteronism (PHA) is the most common form of secondary hypertension of hormonal origin. It affects about 10% of all hypertensive patients. It is connected with increased morbidity and mortality from cardiovascular diseases (CVD) compared to patients with essential hypertension of a similar age. Usually, it is an effect of bilateral adrenal hyperplasia (BAH) or aldosterone-producing adenoma (APA), more rare causes of PHA are: unilateral adrenal hyperplasia, aldosterone-producing adrenocortical carcinoma, ectopic aldosterone-producing tumors and familial hyperaldosteronism. Recent genetic studies have thrown a new light on the pathogenesis of PHA, classifying it as a channelopathy. Several mutations within the ion channels encoding genes have been identified. A possible link between primary hyperaldosteronism and polymorphism of aldosterone synthase gene and ion channel genes is still being investigated. In this manuscript, we focus on genetic aspects of primary hyperaldosteronism, and present an up-to-date compilation of available data with the widened pathogenetic approach.

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