Current Hypertension Reviews最新文献

Hypertension is a major public health problem, affecting more than a quarter of the world's population causing serious cardiovascular problems. In recent years, different polymorphisms have been studied and helped to identify some candidate genes and hereditary syndromes associated with the molecular mechanisms involved in the development of hypertension. Therefore, it is important to identify these molecular mechanisms. This review exposes all the genes and polymorphisms that increase or decrease the risk of hypertension in different populations that are related to the renin angiotensin aldosterone system, G protein, salt excretion, aldosterone synthesis, lipid metabolism, mechanism of insulin resistance, vitamin metabolism, purines and sodium reabsorption. This document can be a useful tool in clinical practice, in addition to serving as a support for future research on this topic.

Background: Preeclampsia (PE) is a pregnancy complication with serious maternal and neonatal consequences worldwide. Our understanding of PE pathophysiology has significantly evolved over the last decades by recognizing that endothelial dysfunction and systemic inflammation, with an associated angiogenic imbalance, are key pieces of this incomplete puzzle. In the present era, where no single treatment to cure or treat this obstetric condition has been developed so far, PE prevention and early prediction are the most useful clinical approach to reduce the PE burden.

Introduction: Although most PE episodes occur in healthy nulliparous women, the identification of specific clinical conditions that increase the risk of PE dramatically provides a critical opportunity to improve outcomes by acting on potentially reversible factors, and also contributes to better understand this pathophysiologic enigma.

Methods: Pertinent studies were searched in PubMed/Medline and Google Scholar (updated August 2020) using common keywords applied in the field of preeclampsia, inflammation and endothelial dysfunction. Given the design of this work as a narrative review, no formal criteria for study selection or appraisal were utilized.

Conclusion: In this review, we highlight major clinical contributors of PE and shed light on their potential link with endothelial dysfunction and inflammation.

The production of renin by the principal cells of the collecting duct has widened our understanding of the regulation of intrarenal angiotensin II (Ang II) generation and blood pressure. In the collecting duct, Ang II increases the synthesis and secretion of renin by mechanisms involving the activation of Ang II type 1 receptor (AT1R) via stimulation of the PKCα, Ca²⁺, and cAMP/PKA/CREB pathways. Additionally, paracrine mediators, including vasopressin (AVP), prostaglandins, bradykinin (BK), and atrial natriuretic peptide (ANP), regulate renin in principal cells. During Ang II-dependent hypertension, despite plasma renin activity suppression, renin and prorenin receptor (RPR) are upregulated in the collecting duct and promote de novo formation of intratubular Ang II. Furthermore, activation of PRR by its natural agonists, prorenin and renin, may contribute to the stimulation of profibrotic factors independent of Ang II. Thus, the interactions of RAS components with paracrine hormones within the collecting duct enable tubular compartmentalization of the RAS to orchestrate complex mechanisms that increase intrarenal Ang II, Na+ reabsorption, and blood pressure.

For all lives regardless of sex, the longitudinal increase in blood pressure (BP) with age is attributed to lifestyle, internal environments like systemic brain-derived neurotrophic factor (BDNF) signaling, and external environments, allowing the individuals to better adapt to the developmental and environmental changes. Basic levels of renin-angiotensin-aldosterone system (RAAS) components in males and females define the fundamental sex difference in BP, which may be set by prenatal programming and the profound influence of BP after birth. The innate sex difference in BP is magnified during puberty growth and later on, affected and modified by menopause in women. At the age of 70 and older, blood pressure has been found to be similar for men and women. Understanding the prenatal setup and development of sexual dimorphism in BP may provide preventative therapeutic strategies, including timing and choice of drugs, for individuals with abnormal BP.

Background: Polymeric nanomaterials with sizes ranging from 10 to 1000 nm are one of the most widely used types of nanoparticles with ideal properties in the drug delivery systems. Here, we decided to systematically review the antihypertensive effects of polymeric nanomaterials in vitro, in vivo, and clinical trials.

Methods: The present review was conducted based on the 06- PRISMA guideline; whereas five English databases, including Scopus, PubMed, Web of Science, EMBASE, and Google Scholar without time limitation were used for searching the publications related to antihypertensive effects of natural and synthetic polymeric nanoparticles.

Results: The results demonstrated that among 1701 papers, 25 papers including 11 in vitro (44%), 6 in vivo (24%), 7 in vitro / in vivo (28%), and 1 in vitro / ex vivo (4%) up to 2020, met the inclusion criteria for discussion in this systematic review. The most used nanoparticles were poly-(lactic- co-glycolic) acid nanoparticle (PLGANPs) (7, 29.2%), chitosan based nanoparticles (6, 25%), followed by polylactide acid nanoparticles (5, 20.8%).

Conclusion: We concluded that the high potency of polymeric nanoparticles in the drug delivery system was for hypertension treatment. Although the accurate mechanisms are not fully understood; however, some mechanisms, such as sustained release forms with increased bioavailability, increasing oral bioavailability and improving the oral and non-oral absorption, counteracting excessive superoxide and decreasing blood pressure, etc. can be related to these nanoparticles.

Background: Recent studies suggested that patients with coronavirus disease 2019 (COVID-19) who use renin-angiotensin system (RAS) inhibitors have an increased risk of respiratory failure and death. The hypothesis was that angiotensin-converting enzyme inhibitor (ACEIs) or angiotensin receptor blocker (ARBs) might up-regulate ACE2 expression that is used as a receptor for viral entry into cells.

Objective: The purpose of this review is to discuss the existing evidence on the interaction between COVID-19 infection, ACE2 and ACEIs or ARBs and to examine the main implications for clinical practice. In addition, novel therapeutic strategies for blocking ACE2-mediated COVID-19 infection will be displayed.

Methods: We performed a comprehensive review of the literature to identify data from clinical and experimental studies for the association between COVID-19 infection, ACE2 and RAS inhibition.

Results: The current clinical and experimental evidence for ACEIs or ARBs to facilitate severe acute respiratory distress syndrome-coronavirus-2 (SARS-CoV-2) is insufficient to suggest discontinuing these drugs. Several observational studies arrive at the conclusion that the continued use of RAS inhibitors is unlikely to be harmful in COVID-19-positive patients.

Conclusions: Further randomized trials are needed to answer the question of whether RAS inhibitors are harmful or beneficial to patients with COVID-19.

Background: The assessment of the longitudinal component of left ventricular (LV) function is of major clinical importance for the early detection of LV contractile impairment. The aim of this study was to determine the impact of uncontrolled hypertension, on LV longitudinal systolic performance.

Methods: The study population included 400 hypertensive patients: 271 patients with uncontrolled blood pressure (BP) and 112 without controlled BP, all patients underwent a complete ultrasound evaluation with the calculation of the LV mass, evaluation of diastolic function as well as longitudinal systolic function.

Results: Conventional echo demonstrated that uncontrolled patients had increased LV mass (P 0.007), LA (left auricular) dimension (P 0.004), left ventricular wall thickness and impairment of diastolic function (E/E'6 ± 2.1 vs 7.4 ±3.0 P=0.001) while no affection of systolic function could be detected. By deformation imaging, there was a reduction in longitudinal strain (apical 4 view -16.2 ±2.9 vs -18.2± 2.6 P 0.02, apical 3 view -17.3 ± 3.3 vs. -18.9 ± 4.1 P 0.01). Similarly, systolic strain rate (SRsys) and early diastolic SR (SRe) reduced significantly in longitudinal direction.

Conclusion: Although EF was not different between uncontrolled patients and controls, LV longitudinal strain and strain rate by 2D speckle tracking were lower in the uncontrolled group.

Background: As a syndrome of physiological vulnerability and multifactorial progressive decline tightly related to age, frailty has been associated with several illnesses, and in particular cardiovascular disease.

Objective: To assess the factors associated with the frailty syndrome in older adults evaluated in the outpatient clinic of a tertiary hospital from Maracaibo city, Venezuela.

Materials and methods: An observational, analytical, cross-sectional study was performed on subjects of both genders, over 60 years old that went to the Internal Medicine outpatient clinic of the Hospital General del Sur "Dr. Pedro Iturbe" from Maracaibo city, Venezuela. Sampling was performed via a non-probabilistic, intentional method. For each subject with frailty or pre-frailty, a control subject was selected in a 1:1 ratio according to gender; several risk factors were interrogated. The state of frailty was determined through the FRAIL scale.

Results: Of the 201 assessed patients, 49.3% (n=99) were non-frail, 19.9% (n=40) were pre-frail and 30.8% (n=62) were frail. The population's overall age was 68.8±6.8 in non-frails, 69.1±7.7 in pre-frails, and 68.6±7.1 in frails. In the multivariate analysis, subjects with frailty and pre-frailty were most likely to be receiving polypharmacy (OR: 2.36, CI95%: 1.05-5.37; P=0.04) and have hypertension during the study (OR: 10.19, CI95%: 3.86-26.89; P<0.01).

Conclusion: The newly diagnosed hypertension and presence of polypharmacy were the factors most associated with frailty and pre-frailty in older adults evaluated in a tertiary hospital from Maracaibo city, Venezuela.

Background: This review explores the mechanistic action of angiotensin-converting enzyme- 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) in the renin-angiotensinaldosterone system (RAAS) that predisposes hypertensive patients to the adverse outcome of severe COVID-19.

Methods and results: Entry of SARS-CoV-2 into the host cell via ACE2 disrupts the RAAS system, creating an imbalance between ACE and ACE2, with an increased inflammatory response, leading to hypertension (HTN), pulmonary vasoconstriction and acute respiratory distress. SARSCoV- 2 may also predispose infected individuals with existing HTN to a greater risk of severe COVID-19 complications. In the duality of COVID-19 and HTN, the imbalance of ACE and ACE2 results in an elevation of AngII and a decrease in Ang (1-7), a hyperinflammatory response and endothelial dysfunction. Endothelial dysfunction is the main factor predisposing hypertensive patients to severe COVID-19 and vice-versa.

Conclusion: Despite the increase in ACE2 expression in hypertensive SARS-CoV-2 infected patients, ARBs/ACE inhibitors do not influence their severity and clinical outcomes, implicating continued usage. Future large-scale clinical trials are warranted to further elucidate the association between HTN and SARS-CoV-2 infection and the use of ARBs/ACEIs in SARS-CoV-2 hypertensive patients.

The prorenin receptor (PRR) is a complex multi-functional single transmembrane protein receptor that is ubiquitously expressed in organs and tissues throughout the body. PRR is involved in different cellular mechanisms that comprise the generation of Angiotensin II, the activation of Wnt/β-catenin signaling, the stimulation of ERK 1/2 pathway, and the proper functioning of the vacuolar H+-ATPase. Evidence supports the role of PRR and its soluble form, sPRR, in the classical features of the metabolic syndrome, including obesity, hypertension, diabetes, and disruption of lipid homeostasis. This review summarizes our current knowledge and highlights new advances in the pathophysiological function of PRR and sPRR in adipogenesis, adipocyte differentiation, lipolysis, glucose and insulin resistance, lipid homeostasis, energy metabolism, and blood pressure regulation.