Current Hypertension Reports最新文献

Purpose of review: The role and underlying mechanisms mediated by dietary salt in modulating the gut microbiota and contributing to heart failure (HF) are not clear. This review summarizes the mechanisms of dietary salt and the gut-heart axis in HF.

Recent findings: The gut microbiota has been implicated in several cardiovascular diseases (CVDs) including HF. Dietary factors including high consumption of salt play a role in influencing the gut microbiota, resulting in dysbiosis. An imbalance of microbial species due to a reduction in microbial diversity with accompanying immune cell activation has been implicated in the pathogenesis of HF via several mechanisms. The gut microbiota and gut-associated metabolites contribute to HF by reducing gut microbiota biodiversity and activating several signaling pathways. High dietary salt modulates the gut microbiota composition and exacerbate or induce HF by increasing the expression of the epithelial sodium/hydrogen exchanger isoform 3 in the gut, cardiac expression of beta myosin heavy chain, activation of the myocyte enhancer factor/nuclear factor of activated T cell, and salt-inducible kinase 1. These mechanisms explain the resulting structural and functional derangements in patients with HF.

Puberty is a complex process leading to physical, sexual, and psychosocial maturation. The changes in morphology and organ function during puberty also affect blood pressure (BP) regulation, and as a consequence (BP) values change noticeably, reaching values often higher than after reaching full maturity. In children entering puberty, BP, especially systolic, increases and then reaches adult values by the end of puberty. The mechanisms responsible for this process are complex and not fully understood. Sex hormones, growth hormone, insulin-like growth factor-1, and insulin, whose production increases during puberty, significantly regulate BP through complex and overlapping mechanisms. During puberty, the incidence of arterial hypertension also increases, especially in children with excess body weight. The present paper presents the current state of knowledge regarding the influence of processes occurring during puberty on blood pressure.

Purpose of review: The response to natural stressors involves both cardiac stimulation and vascular changes, primarily triggered by increases in sympathetic activity. These effects lead to immediate flow redistribution that provides metabolic support to priority target organs combined with other key physiological responses and cognitive strategies, against stressor challenges. This extremely well-orchestrated response that was developed over millions of years of evolution is presently being challenged, over a short period of time. In this short review, we discuss the neurogenic background for the origin of emotional stress-induced hypertension, focusing on sympathetic pathways from related findings in humans and animals.

Recent findings: The urban environment offers a variety of psychological stressors. Real or anticipatory, emotional stressors may increase baseline sympathetic activity. From routine day-to-day traffic stress to job-related anxiety, chronic or abnormal increases in sympathetic activity caused by emotional stressors can lead to cardiovascular events, including cardiac arrhythmias, increases in blood pressure and even sudden death. Among the various alterations proposed, chronic stress could modify neuroglial circuits or compromise antioxidant systems that may alter the responsiveness of neurons to stressful stimuli. These phenomena lead to increases in sympathetic activity, hypertension and consequent cardiovascular diseases. The link between anxiety, emotional stress, and hypertension may result from an altered neuronal firing rate in central pathways controlling sympathetic activity. The participation of neuroglial and oxidative mechanisms in altered neuronal function is primarily involved in enhanced sympathetic outflow. The significance of the insular cortex-dorsomedial hypothalamic pathway in the evolution of enhanced overall sympathetic outflow is discussed.

Purpose of review: Accumulating data on the consumption of plant-based diets and their impact on blood pressure indicate a consensus that plant-based diets are linked to reduced blood pressure. The suggested mechanisms of action are manifold, and, in this systematic review, we provide a summary of the most recent findings on plant-based diets and their impact on blood pressure, along with an analysis of the molecules accountable for the observed effects.

Recent findings: The overwhelming majority of intervention studies demonstrate that plant-based diets result in lower blood pressure readings when compared to diets that are based on animal products. The various mechanisms of action are being clarified. The data discussed in this systematic review allow us to conclude that plant-based diets are associated with lower blood pressure and overall better health outcomes (namely, on the cardiovascular system) when compared to animal-based diets. The mechanisms of action are being actively investigated and involve many macro- and micronutrients plentiful in plants and the dishes prepared with them.

Purpose of review: Preeclampsia (PE) is a leading global cause of maternal and fetal morbidity and mortality. The heterogeneity of this disorder contributes to its elusive etiology. Due to the ethical constraints surrounding human studies, animal models provide a suitable alternative for investigation into PE pathogenesis and novel therapeutic strategies. The purpose of this review is to compare and contrast the various rodent models used to study PE, in order to demonstrate their value in investigating and identifying different characteristics of this disorder.

Recent findings: Several approaches have been employed to create an appropriate animal model of PE, including surgical, genetic manipulation, and pharmacological methods in an attempt to mimic the maternal syndrome. Despite the absence of a model to completely model PE, these models have provided valuable information concerning various aspects of PE pathogenesis and novel therapeutic strategies and have led to the discovery of potential predictive markers of PE. Rodent and murine models have contributed significantly to the study of the pathology associated with specific aspects of the disorder. As a single fully encompassing animal model of PE remains absent, the use of a combination of models has potential value in understanding its etiology as well as in new treatment and management strategies.

Purpose of review: This is a pragmatic decision aid for initiating pharmacotherapy for stage 1 hypertension.

Recent findings: If a stage 1 patient presents with clinical signs of fluid retention, then a diuretic should be the primary agent. However, if the patient is normovolemic, then a vasodilator should be the primary agent. If targeted blood pressure is not achieved with the primary agent, then the choices are dose escalation or the addition of a second drug. For stage 1, the addition of secondary agents is preferred. This approach includes the polypill (a single pill with multiple low-dose antihypertensive agents). The positives are the polypill lessens the need to make decisions associated with up-titration and the low doses mitigate adverse side effects. The polypill targets several concurrent mechanisms to counteract hypertension. For stage 1, the goal should be to lower blood pressure with a simple regiment which minimizes adverse side affects.

Purpose of review: To address the mechanistic pathways focusing on mitochondria dysfunction, oxidative stress, sirtuins imbalance, and other contributors in patient with metabolic syndrome and cardiovascular disease. Sodium glucose co-transporter type 2 (SGLT-2) inhibitors deeply influence these mechanisms. Recent randomized clinical trials have shown impressive results in improving cardiac function and reducing cardiovascular and renal events. These unexpected results generate the need to deepen our understanding of the molecular mechanisms able to generate these effects to help explain such significant clinical outcomes.

Recent findings: Cardiovascular disease is highly prevalent among individuals with metabolic syndrome and diabetes. Furthermore, mitochondrial dysfunction is a principal player in its development and persistence, including the consequent cardiac remodeling and events. Another central protagonist is the renin-angiotensin system; the high angiotensin II (Ang II) activity fuel oxidative stress and local inflammatory responses. Additionally, sirtuins decline plays a pivotal role in the process; they enhance oxidative stress by regulating adaptive responses to the cellular environment and interacting with Ang II in many circumstances, including cardiac and vascular remodeling, inflammation, and fibrosis. Fasting and lower mitochondrial energy generation are conditions that substantially reduce most of the mentioned cardiometabolic syndrome disarrangements. In addition, it increases sirtuins levels, and adenosine monophosphate-activated protein kinase (AMPK) signaling stimulates hypoxia-inducible factor-1β (HIF-1 beta) and favors ketosis. All these effects favor autophagy and mitophagy, clean the cardiac cells with damaged organelles, and reduce oxidative stress and inflammatory response, giving cardiac tissue protection. In this sense, SGLT-2 inhibitors enhance the level of at least four sirtuins, some located in the mitochondria. Moreover, late evidence shows that SLGT-2 inhibitors mimic this protective process, improving mitochondria function, oxidative stress, and inflammation. Considering the previously described protection at the cardiovascular level is necessary to go deeper in the knowledge of the effects of SGLT-2 inhibitors on the mitochondria function. Various of the protective effects these drugs clearly had shown in the trials, and we briefly describe it could depend on sirtuins enhance activity, oxidative stress reduction, inflammatory process attenuation, less interstitial fibrosis, and a consequent better cardiac function. This information could encourage investigating new therapeutic strategies for metabolic syndrome, diabetes, heart and renal failure, and other diseases.

Purpose of review: To describe the physiological aspects of blood pressure and arterial stiffness, as well as explain how these processes are related. To review the available evidence on the effect of treatment with different classes of antihypertensive drugs on improving arterial stiffness.

Recent findings: Specific classes of antihypertensive drugs may have effects directly on improving arterial stiffness independent of lowering blood pressure. The maintenance of normal blood pressure levels is essential for the homeostasis of the whole organism; the increase in blood pressure is directly related to the increased risk of cardiovascular diseases. Hypertension is characterized by structural and functional changes in blood vessels and is associated with a more accelerated progression of arterial stiffness. Randomized clinical trials have shown that some specific classes of antihypertensive drugs can improve arterial stiffness independently of their effect on lowering brachial blood pressure. These studies show that calcium channel blockers (CCBs), angiotensin II receptor blockers (ARBs), and angiotensin-converting enzyme (ACE) inhibitors have been shown to have a better effect on arterial stiffness compared to diuretics and beta-blockers in individuals with arterial hypertension and other cardiovascular risk factors. More real-world studies are needed to assess whether this effect on arterial stiffness can improve the prognosis of patients with hypertension.

Purpose of review: To review the current literature regarding hypertension (HTN) following pediatric solid organ transplant (SOTx), including definition, prevalence, risk factors, outcomes, and treatment.

Recent findings: In recent years several new guidelines for the definition, monitoring, and management of pediatric HTN have been published, but with no specific recommendations regarding SOTx recipients. HTN remains highly prevalent, yet underdiagnosed and undertreated in kidney transplant (KTx) recipients, especially when ambulatory blood pressure monitoring (ABPM) is utilized. There are little data regarding its prevalence in other SOTx recipients. HTN in this population is multifactorial and is associated with HTN status prior to Tx, demographic factors (age, sex, and race), weight status, and immunosuppression protocol. HTN is associated with subclinical cardiovascular (CV) end-organ damage, including left ventricular hypertrophy (LVH) and arterial stiffness, yet there are no recent data regarding its long-term outcomes. There are also no updated recommendations regarding the optimal management of HTN in this population. Given its high prevalence and the young age of this population facing years at increased CV risk, post-Tx HTN requires more clinical attention (routine monitoring, frequent application of ABPM, better BP control). Additional research is needed for a better understanding of its long-term outcomes as well as its treatment and treatment goals. Much more research is needed regarding HTN in other pediatric SOTx populations.

Purpose of review: Hypertension is the primary risk factor for cardiovascular disease and adequate blood pressure control is often elusive. The objective of this work was to conduct a meta-analysis of trial data of isometric resistance training (IRT) studies in people with hypertension, to establish if IRT produced an anti-hypertensive effect. A database search (PubMed, CINAHL, Cochrane Central Register of Controlled Trials, and MEDLINE) identified randomised controlled and crossover trials of IRT versus a sedentary or sham control group in adults with hypertension.

Recent findings: We included 12 studies (14 intervention groups) in the meta-analyses, with an aggregate of 415 participants. IRT reduced systolic blood pressure (SBP), mean difference (MD) - 7.47 mmHg (95%CI - 10.10, - 4.84), P < 0.01; diastolic blood pressure (DBP) MD - 3.17 mmHg (95%CI - 5.29, - 1.04), P < 0.01; and mean arterial blood pressure (MAP) MD - 7.19 mmHg (95%CI - 9.06, - 5.32), P < 0.0001. Office pulse pressure and resting heart rate was not significantly reduced, neither were 24-h or day-time ambulatory blood pressures (SBP, DBP). Night-time blood pressures, however, were significantly reduced with SBP MD - 4.28 mmHg (95%CI - 7.88, - 0.67), P = 0.02, and DBP MD - 2.22 mmHg (95%CI - 3.55, - 0.88), P < 0.01. IRT does lower SBP, DBP and MAP office and night-time ambulatory SBP and DBP, but not 24-h mean ambulatory blood pressures in people with hypertension.