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Background: Arterial hypertension in children is considered a common alteration nowadays, mainly because obesity is a growing worldwide problem closely related to increased blood pressure. Childhood hypertension can be classified as primary or secondary, depending on the etiology. Primary or essential hypertension still has its pathophysiology not fully elucidated, and there is no consensus in the literature on most underlying mechanisms. In this review, genetic and environmental factors, including sodium and potassium intake, socioeconomic status, ethnicity, family structure, obesity, sedentary lifestyle, prematurity and low birth weight, prenatal and postnatal exposures are highlighted., Objective: The present study aimed to perform an update on primary hypertension in childhood, providing clinicians and researchers an overview of the current state of the literature regarding the influence of genetic and environmental factors., Methods: This integrative review searched for articles on genetic and environmental factors related to primary hypertension in pediatric patients. The databases evaluated were PubMed and Scopus., Results: The studies have provided insights regarding many genetic and environmental factors, in addition to their association with the pathophysiology of primary hypertension in childhood. Findings corroborated the idea that primary hypertension is a multifactorial disease. Further studies in the pediatric population are needed to elucidate the underlying mechanisms., Conclusion: The study of primary hypertension in pediatrics has utmost importance for the adoption of preventive measures and the development of more efficient treatments, therefore reducing childhood morbidity and the incidence of cardiovascular diseases and other health consequences later in life., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Angiotensin II is a potent activator of the Rho-kinase (ROCK) pathway, through which it exerts some of its adverse vasoconstrictor effects. Clinical evidence on the effects of blocking the angiotensin II receptor 1 on ROCK activity in hypertensive patients is scarce., Objective: To demonstrate that ROCK activity in peripheral blood mononuclear cells (PMBCs) in patients with essential hypertension is reduced earlier than previously observed, along with blood pressure (BP) lowering on treatment with olmesartan., Methods: Prospective pilot open study; 17 hypertensive patients were treated with progressive olmesartan doses starting with 20 mg qd. BP was measured at 3, 6 and 9 weeks after treatment initiation. If treatment failed to normalize BP after 3 weeks, olmesartan dose was increased to 40 mg qd, and if still hypertensive after 6 weeks, 12.5 mg of hydrochlorothiazide qd was added. ROCK activity was measured at baseline and 9 weeks after treatment as myosin phosphatase target subunit 1 phosphorylation (MYPT1-p/T ratio) in PBMC., Results: Mean baseline BP was 162 ± 4.9/101 ± 2.4 mmHg. After 9 weeks of treatment, both systolic and diastolic BP were reduced by 41 and 22 mmHg, respectively (p<0.05). Mean pretreatment MYPT1- p/T ratio in PMBCs was significantly reduced by 80% after 9 weeks with olmesartan (p<0.01)., Conclusion: Normotension achieved after 9 weeks in 82% of the patients treated with olmesartan was associated with a significant reduction of ROCK activity in PBMC., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Advances in treatment and increased awareness have improved the prognosis for many patients with hypertension (HTN). Resistant hypertension (RH) refers to a subset of hypertensive individuals who fail to achieve a desired blood pressure (BP) despite concurrent use of 3 different classes antihypertensive agents, one being a diuretic, and proper lifestyle changes. The prevalence and prognosis of RH are unclear owing to its heterogeneous etiologies, risk factors, and secondary comorbidities. Previous research has provided evidence that increased renal sympathetic nerve activity (RSNA) within the renal artery contributes to RH development. Renal denervation (RDN) is a procedure that attempts to ameliorate the effects of heightened RSNA via ablation renal sympathetic fibers. BP reductions associated with RDN may be attributed to decreased norepinephrine spillover, restoration of natriuresis, increasing renal blood flow, and lowering plasma renin activity. Early clinical trials perpetuated positive results, and enthusiasm grew exponentially. However, recent clinical trials have called into question RDN's efficacy. Numerous limitations must be addressed to discern the true effectiveness of RDN as a therapeutic option for RH., Objective: We aimed to review the current understanding of RH, the anatomy of renal arteries, physiology of RH on renal arteries, anatomical pathways of the sympathetic involved in RH, RDN as a treatment option, and all relevant clinical trials treating RH with RDN., Methods: We piloted a MEDLINE® database search of literature extending from 1980 to 2017, with emphasis on the previous five years, combining keywords such as "resistant hypertension" and "renal denervation.", Conclusion: A plethora of information is available regarding heightened RSNA leading to RH. RDN as a possible treatment option has shown a range of results. Reconciling RDN's true efficacy requires future trials to increased sites of nerve ablation, standardized protocol, increased anatomical understanding per individual basis, stricter guidelines regarding study design, increased operator experience, and integrating the use of a multielectrode catheter., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Objectives: Accumulating evidence suggests a direct role of Uric Acid (UA) on Left Ventricular (LV) diastolic function in chronic kidney disease and Heart Failure (HF) patients. Recently, UA has been linked to LV Hypertrophy (LVH) and Diastolic Dysfunction (DD) in women with preserved Ejection Fraction (pEF) but not in corresponding men. We sought to assess if UA could predict indices of DD in hypertensive subjects with pEF independently of gender., Method: We consecutively recruited 382 apparently healthy hypertensive subjects (age: 61.7±10.7, women: 61.3%, median EF: 64%). In 318 patients in sinus rhythm, LV mass-indexed to body surface area-was calculated (LVMI). LVH was set as an LVMI >116g/m2 or 96 g/m2 in men and women, respectively. The ratio of early transmitral peak velocity (E) to the mitral annular early diastolic velocity (Em) was used as an approximation of mean left atrial pressure (E/Em)., Results: UA [median (interquartile range): 5.4(2) mg/dl] independently predicted E/Em (adjusted coefficient: 1.01, p =0.026) while an interaction term between gender and UA was no significant (p=0.684). An ordinal score of DD was calculated taking into account increased E/Em, left atrium dilatation and LVH. Women with increased UA had 254% increased odds (adjusted OR=2.54, p=0.005) to be classified in the upper range of the DD score., Conclusion: In hypertensive subjects without HF, UA is independently associated with the presence of DD in both genders and correlates with its severity in women. Further prospective studies are warranted to evaluate the association of UA with adverse cardiovascular outcomes in high-risk populations such as HF with pEF., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

Background: Patients with hypertension have altered autonomic nervous system function, which are increased sympathetic activity. Transcutaneous Electrical Nerve Stimulation (TENS) is a useful modality for pain control and has also been shown to be effective in the reduction of sympathetic activity in healthy subjects and individuals with cardiovascular diseases., Objective: The aim of this study was to verify the effects of transcutaneous electrical nerve stimulation by the evaluation of heart rate variability (HRV) in patients with essential hypertension., Method: Twenty-eight patients received an application of low-frequency TENS(4 Hz) n=8, highfrequency TENS (100 Hz) n=10 or placebo TENS n=10 in paravertebral ganglionar region during thirty minutes., Results: After 4 Hz TENS, there was a decrease in the low-frequency (LFn.u.) component (57.71±9.46 vs 45.58±13.51, p<0.026) and an increase in the high-frequency (HFn.u.) component (33.03±13.83 vs 45.83±20.19, p <0.05) of HRV. After 100 Hz TENS and placebo, there were no changes in the LF and HF components. No significant differences were found in systolic blood pressure with low-frequency TENS (129.37± 15.48 vs 126.69 ± 15.21, p<0.490). There was an increase, although not significant, with high-frequency TENS (131.00 ± 15.97 vs 138.75 ± 25.79, p<0.121) and placebo (133.80 ± 29.85 vs 134.80 ± 29.72, p< 0.800). No differences were found in the diastolic blood pressure with low-frequency TENS and placebo, but there was a significant increase in high-frequency TENS (81.00 ± 11.78 vs 85.65 ± 13.68, p< 0.018)., Conclusion: Low-frequency TENS decreases sympathetic nervous system activity and increases parasympathetic nervous system activity and high-frequency TENS increases diastolic blood pressure, when applied on the paravertebral ganglionar region in the hypertensive patients., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

Introduction: Chronic serum uric acid elevation (SUA) is known to be induced by dyslipidemia, hypertension, inflammation, and insulin resistance. Therefore, it has been associated with higher risk for coronary artery disease and cardiovascular mortality. Also, increased levels of SUA have been associated with regional arterial stiffness, assessed by pulse wave velocity (PWV)., Aims: To evaluate the relationships of PWV, SUA and different metabolic parameters in essential hypertensive patients., Material and Methods: We evaluated 445 essential hypertensive patients, by measuring office blood pressure (BP), weight, height, and waist circumference. In each patient, blood samples were drawn for biochemical evaluations and 24h urine collection. Body Mass Index (BMI) and Glomerular Filtration Rate (GFR) were calculated. Carotid-Femoral PWV and Left Ventricular Mass Index (LVMI) were measured in all patients., Results: All subjects (n=402), 242 males (55±0.9 yrs.; BMI: 28.9±0.3 Kg/m2) and 160 females (58±1 yrs.; BMI: 28.1±0.4 Kg/m2) had normal renal function. PWV values showed a significant association with SUA (p<0.001), Systolic BP (p<0.025) and LVMI (p<0.05). SUA showed a significant association, p<0.025: with BMI, Waist Circumference, and HDL-C; p<0.05: with Glycaemia at 120 min, Insulin at 120 min, TG, and LVMI; and p<0.001: with serum Creatinine. Backward Stepwise Regression showed that PWV could be predicted from SUA (p<0.001) and Systolic BP (p<0.05). BMI, Waist Circumference, DBP and HR did not significantly add to the ability of the equation to predict PWV., Conclusions: In this population of essential hypertensive patients, SUA was associated to increased arterial stiffness and to components of the Metabolic Syndrome. These results raise the possibility that a new approach to the role of SUA, linked to cardiovascular stratification, and a most appropriate treatment might be considered., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

Background: Ambulatory Arterial Stiffness Index (AASI) has been proposed as an indirect and simpler method to estimate the Arterial Stiffness (AS). AASI, calculated from a set of data collected during a 24-hours ambulatory blood pressure monitoring (ABPM), is defined as 1 minus the regression slope of diastolic on systolic blood pressure (BP) values. For a given increase in diastolic BP, the increase in systolic BP is smaller in a compliant compared to a stiff artery; the stiffer the arterial tree, the closer AASI is to 1. AASI was demonstrated to predict cardiovascular mortality, cerebrovascular events and to be associated with target organ damage. Taking into account the almost complete absence of data regarding the ability of AASI to predict the different degree of AS when hypertensives are divided into four classes of dipping in relation to the extent of the nocturnal reduction of BP (extreme dippers, dippers, mild dippers and reverse dippers) aim to clarify the ability of AASI to estimate the different degree of AS of hypertensive subjects with different nocturnal BP profile and resulting in different extent of organ damage., Materials and Methods: We enrolled 816 subjects (403 men and 413 women) with essential hypertension, referred to the U.O.C of Medicina Interna e Cardioangiologia of the University of Palermo; 173 subjects (71 men and 102 women, mean age 44.4 ± 14.6 years) without a history of hypertension were enrolled as controls., Results: The analysis of data was performed by dividing the population into four categories in relation to the extent of the nocturnal decline of BP: 124 extreme dipper (mean age 54,8 ± 12,4 years, men 46.8 %); 287 dipper (mean age 55,9 ± 14,2 years, men 54,0 %); 271 mild dipper (mean age 61,5 ± 14,7 years, men 52,0 %); 134 reverse dipper (mean age 61,5 ± 14,7 years, men 33.6 %). The mean value of AASI was significantly higher for mild and reverse dippers versus control patients and versus the other categories of dipping. The multiple regression analysis with AASI as the dependent variable confirmed the significant association between AASI and nocturnal dip (p: 0.015). The Multinomial Logistic Regression Analysis, in which AASI values were adjusted for the main confounders (age, sex, Body Mass Index, 24h SBP, 24h DBP) showed that the association between AASI and dipping is maintained only for dipper and extreme dipper hypertensives, missing the significance for mild and reverse subjects., Conclusion: 1) AASI levels are associated with night-to-day BP ratio; 2) Lower levels of AASI are significantly associated to extreme dipper and dipper BP nocturnal profile when compared to healthy controls. 3) After correction for the major confounding factors, the association between AASI and the high-damaged class of hypertensive subjects with lower or no nocturnal fall of BP is lost. Our findings support the hypothesis that AASI is unable to estimate AS of older hypertensive subjects with a high burden of organ and vascular damage and several comorbidities, probably because the nocturnal reduction of BP is the main determinant of AASI, being more powerful than AS itself., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)