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Heart failure is a prevalent disease worldwide. While it is well accepted that heart failure involves changes in myocardial energetics, what alterations that occur in fatty acid oxidation and glucose oxidation in the failing heart remains controversial. The goal of the study are to define the energy metabolic profile in heart failure induced by obesity and hypertension in aged female mice, and to attempt to lessen the severity of heart failure by stimulating myocardial glucose oxidation. 13-Month-old C57BL/6 female mice were subjected to 10 weeks of a 60% high-fat diet (HFD) with 0.5 g/L of Nω-nitro-L-arginine methyl ester (L-NAME) administered via drinking water to induce obesity and hypertension. Isolated working hearts were perfused with radiolabeled energy substrates to directly measure rates of myocardial glucose oxidation and fatty acid oxidation. Additionally, a series of mice subjected to the obesity and hypertension protocol were treated with a pyruvate dehydrogenase kinase inhibitor (PDKi) to stimulate cardiac glucose oxidation. Aged female mice subjected to the obesity and hypertension protocol had increased body weight, glucose intolerance, elevated blood pressure, cardiac hypertrophy, systolic dysfunction, and decreased survival. While fatty acid oxidation rates were not altered in the failing hearts, insulin-stimulated glucose oxidation rates were markedly impaired. PDKi treatment increased cardiac glucose oxidation in heart failure mice, which was accompanied with improved systolic function and decreased cardiac hypertrophy. The primary energy metabolic change in heart failure induced by obesity and hypertension in aged female mice is a dramatic decrease in glucose oxidation. Stimulating glucose oxidation can lessen the severity of heart failure and exert overall functional benefits., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.)

A diagnostic of hypertension increases the risk of erectile dysfunction (ED); likewise, ED can be an early sign of hypertension. In both cases, there is evidence that endothelial dysfunction is a common link between the 2 conditions. During hypertension, the sustained and widespread release of procontractile factors (e.g., angiotensin II, endothelin 1, and aldosterone) impairs the balance between vasoconstrictors and vasodilators and, in turn, detrimentally impacts vascular and erectile structures. This prohypertensive state associates with an enhancement in the generation of reactive oxygen species, which is not compensated by internal antioxidant mechanisms. Recently, the innate immune system, mainly via Toll-like receptor 4, has also been shown to actively contribute to the pathophysiology of hypertension and ED not only by inducing oxidative stress but also by sustaining a low-grade inflammatory state. Furthermore, some drugs used to treat hypertension can cause ED and, consequently, reduce compliance with the prescribed pharmacotherapy. To break down these challenges, in this review, we focus on discussing the well-established as well as the emerging mechanisms linking hypertension and ED with an emphasis on the signaling network of the vasculature and corpora cavernosa, the vascular-like structure of the penis., (© American Journal of Hypertension, Ltd 2020. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

The immune system plays a prominent role in the initiation and maintenance of hypertension. The innate immune system, via toll-like receptors (TLRs), identifies distinct signatures of invading microbes and damage-associated molecular patterns and triggers a chain of downstream signalling cascades, leading to secretion of pro-inflammatory cytokines and shaping the adaptive immune response. Over the past decade, a dysfunctional TLR-mediated response, particularly via TLR4, has been suggested to support a chronic inflammatory state in hypertension, inducing deleterious local and systemic effects in host cells and tissues and contributing to disease progression. While the underlying mechanisms triggering TLR4 need further research, evidence suggests that sustained elevations in BP disrupt homeostasis, releasing endogenous TLR4 ligands in hypertension. In this review, we discuss the emerging role of TLR4 in the pathogenesis of hypertension and whether targeting this receptor and its signalling pathways could offer a therapeutic strategy for management of this multifaceted disease. LINKED ARTICLES: This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc., (© 2018 The British Pharmacological Society.)

Objectives: to identify the degree of knowledge of people with hypertension concerning the disease and to verify the factors associated with the non-adherence to anti-hypertensive drug therapy., Method: Cross sectional study, involving 422 people. Data collection took place at their homes, between December 2011 and March 2012, through interviews using the following instruments: Medication Adherence Questionnaire (MAQ-Q), Medication Regimen Complexity Index (MRCI) and a guide with questions related to sociodemographic profile, satisfaction with healthcare service and knowledge about the disease., Results: 42.6% did not adhere to the drug therapy and 17.7% had poor knowledge about the disease. Factors associated with the non-adherence were: complex drug therapy, poor knowledge about the disease and dissatisfaction with the healthcare service., Conclusion: The findings reinforce that the complex drug therapy prescriptions, little knowledge about the disease and dissatisfaction with the healthcare service have influence on the process of non-adherence to anti-hypertensive drug therapy.

Introduction: The detection of the renal artery stenosis in hypertensive patients can be a signal of systemic arterial atherosclerosis., Aims: To identify and characterize clinical-epidemiologically the hypertensive patients with renal artery stenosis, evaluating factors of cardiovascular risk and presence of symptomatic multiarterial atherosclerotic., Method: Were selected the hypertensive patients who were assisted at the Nephrological Clinic of Universidade Federal do Triângulo Mineiro (UFTM) between 2000-2010, with diagnosis of renal artery stenosis of atherosclerotic etiology. Epidemiological data were evaluated (gender, age, ethnicity), factors of cardiovascular risk (diabetes, hypercholesterolemia, hypertriglyceridemia, tabagism, metabolic syndrome), information on hypertension (time of diagnosis, family report, number of used medicines), previous cardiovascular events (acute myocardial infarctation, ischemic stroke, peripheral arterial disease). Blood pressure levels, global cardiovascular risk and Score Framingham were stratified., Results: Casuistry of 30 patients, feminine majority (73.3%), average of 66 year-old age, 86.67% white, medium time of hypertension of 19.94 years, 89.92 without family report, 13.8 with diabetes, 65.51% smoking, 17.25% hypertriglyredemia, 62.06% with hypercholesterolemia and 66.7% with metabolic syndrome. Average number of medicines in use: 3.26. Dominant right-sided renal artery stenosis separately (46.7%) and in proximal third (56.7%). High creatinine levels in 40% of the patients. As for the hypertension phase, majority phase 2 (47%) and 73.3% with high global cardiovascular risk. Average Framingham Score of 13%. 66.7% presented atherosclerotic disease in another place, being infarctation the main one (53.3%)., Conclusion: The most common correlation was with acute myocardial infarctation, what implicates in the search of the coronary compromising to the diagnosis of renal artery stenosis in hypertensive patients to try avoid future damages to the patient.

Descriptive study with qualitative approach that aimed to understand the perspective of health professionals and hypertensive patients on their mutual interaction in the public health context, so as to analyze how this interaction contributes to non-compliance with treatment. Interviews with 15 health professionals and 10 hypertensive patients who interacted in public health units were carried out. In the interaction between the health professional and the hypertensive user, it was concluded that, in order to solve the problem of non-compliance with treatment from the part of the user, the health professional makes use of awareness strategies. In practice, however, this has occurred inappropriately and under the biomedical care model. Users, in turn, have managed treatment their own way, indicating some issues to health professionals regarding compliance.