Misalignment between the endogenous biological timing system and behavioral activities (i.e., sleep/wake, eating, activity) contributes to adverse cardiovascular health. In this review, we discuss the effects of recurring circadian misalignment on blood pressure regulation and the implications for hypertension development. Additionally, we highlight emerging therapeutic approaches designed to mitigate the negative cardiovascular consequences elicited by circadian disruption. Circadian misalignment elicited by work schedules that require individuals to be awake during the biological night (i.e., shift work) alters 24-h blood pressure rhythms. Mechanistically, circadian misalignment appears to alter blood pressure via changes in autonomic nervous system balance, variations to sodium retention, dysregulation of endothelial vasodilatory responsiveness, and activation of proinflammatory mechanisms. Recurring circadian misalignment produced by a mismatch in sleep timing on free days vs. work days (i.e., social jetlag) appears to have no direct effects on prevailing blood pressure levels in healthy adults; though, circadian disruptions resulting from social jetlag may increase the risk of hypertension through enhanced sympathetic activation and/or obesity. Furthermore, social jetlag assessment may be a useful metric in shift work populations where the magnitude of circadian misalignment may be greater than in the general population. Circadian misalignment promotes unfavorable changes to 24-h blood pressure rhythms, most notably in shift working populations. While light therapy, melatonin supplementation, and the timing of drug administration may improve cardiovascular outcomes, interventions designed to target the effects of circadian misalignment on blood pressure regulation are warranted.

This review aims to explore the role of microvascular dysfunction in obesity-hypertension, discuss the effects obesity has on renal microvasculature,reviewthe current methods for assessing microvascular dysfunction and availabletherapeutic options, and identify critical areas for further research. There is a strong association between obesity and hypertension. However, the pathophysiology of obesity-hypertension is not clear. Microvascular dysfunction has been linked to hypertension and obesity and could be an important mediator of obesity-related hypertension. Newer therapies for hypertension and obesity could have ameliorating effects on microvascular dysfunction, including GLP-1 agonists and SGLT-2 inhibitors. There is still much progress to be made in our understanding of the complex interplay between obesity, hypertension, and microvascular dysfunction. Continued efforts to understand microvascular dysfunction and its role in obesity-hypertension are crucial to develop precision therapy to target obesity-hypertension.

Essential hypertension is a huge health problem that significantly impacts worldwide population in terms of morbidity and mortality. Idiopathic in its nature, elevated blood pressure results from a complex interaction between polygenic components and environmental and lifestyle factors. The constant growth in the burden of hypertension is at odds with expectations, considering the availability of therapeutic strategies. Hence, there is an endless need to further investigate the complexity of factors contributing to blood pressure elevation. Recent data indicate that bidirectional interactions between the nervous system and the immune system alter inflammation in the brain and periphery, contributing to chronic hypertension. These findings indicate that the nervous system is both a direct driver of hypertension and also a target of feedback that often elevates blood pressure further. Similarly, the immune system is both target and driver of the blood pressure increases. The contributions of the feedback loops among these systems appear to play an important role in hypertension. Together, recent mechanistic studies strongly suggest that the interactions among the brain, immune system, and inflammation affect the participation of each system in the pathogenesis of hypertension, and thus, all of these systems must be considered in concert to gain a full appreciation of the development and potential treatments of hypertension.

Primary aldosteronism (PA) is a leading global cause of secondary hypertension. Subtyping diagnosis of PA is the key to surgery, but accurate classification of PA is crucial but challenging in clinical diagnosis and treatment. The purpose of this review is to provide a summary of current literature and propose subtyping diagnosis flow chart to help us classify PA quickly and accurately. Early diagnosis and accurate typing are essential for the timely treatment and appropriate management of PA. For most patients, adrenal venous sampling (AVS) is the central choice for typing diagnosis, but AVS is invasive and difficult to promote effectively. CT can help identify unilateral typical adenomas in select patients to avoid AVS. New radionuclide imaging has shown value in the diagnosis and classification of PA, which distinguishes adrenocortical hyperplasia from adenoma and can replace AVS in some patients. Accurately diagnosing unilateral PA is crucial for determining the appropriate treatment strategy for PA. The simple flow chart of PA subtyping diagnosis based on the current literature needs to be verified and evaluated by follow-up researches.

To review the current literature on care of hypertension and chronic kidney disease for people who are currently and formerly incarcerated, and to make recommendations for improving outcomes. There is a growing body of literature describing care for kidney disease and hypertension for incarcerated and formerly incarcerated individuals that documents the provision of care itself, notably that many jails contract with private companies; the system is not designed to provide sustained, chronic disease care; and the transition from incarceration to community is fraught with gaps in care. However, deficiencies in data collection and regulation still limit our understanding of the quality of care provided in jails and prisons. Furthermore, more data is needed to understand the impact of structural racism in the criminal legal system on overall disparities in care for hypertension and kidney disease. Insurance coverage rates for people who were formerly incarcerated continue to be lower than the general population despite Medicaid expansion in many states. There is little recent data regarding kidney replacement therapy for this population despite known variation in dialysis modalities and transplant programs by state. Transitions clinics, which connect people who were formerly incarcerated with care in the community upon release, are growing and are important avenues by which to deliver care. People who are incarcerated are disproportionately affected by hypertension and kidney disease, yet data regarding the extent of these inequities and availability of quality care is lacking. More work is needed to understand the care of individuals with kidney disease and hypertension in prisons and to improve outcomes for these common chronic conditions. Both providing effective treatment of kidney disease and hypertension in prisons and jails and providing coordinated, quality transition to community care upon release represents an important opportunity for reform in care for a marginalized population.

Use of renin-angiotensin-aldosterone system (RAAS) inhibiting medications is critical in the prevention of cardiovascular disease and kidney function decline in patients with chronic kidney disease (CKD); however, these agents can lead to hyperkalemia, an electrolyte disorder associated with risk of arrythmia, conduction disorders, and increased overall mortality. Discontinuation, or reduction of dose, of RAAS inhibitor therapy in hyperkalemic patients with CKD can lead to loss of kidney and cardiovascular protection afforded by these medications. Given the high prevalence of hyperkalemia among patients with CKD utilizing RAAS inhibitors, clear management principles are critical to minimize risk and maximize benefit when facing this clinical dilemma. Strategies to mitigate hyperkalemia that do not interfere with optimal RAAS inhibitor therapy should be prioritized when managing potassium elevation in patients with CKD. These strategies include discontinuing non-RAAS inhibitor medications known to cause hyperkalemia, correction of metabolic acidosis, and maximization of medication therapies that lower serum potassium, including diuretics and sodium-glucose cotransporter-2 (SGLT-2) inhibitors. Initiation of potassium exchange resins should also be considered to allow for sustained RAAS inhibitor utilization. An approach which employs multiple strategies concurrently is important to mitigate hyperkalemia and maintain long-term use of RAAS-inhibitors. Persistence of RAAS inhibitor use in patients with CKD is important to slow kidney function decline, delay onset of dialysis or the need for kidney transplant, and prevent adverse cardiovascular outcomes. When hyperkalemia develops among patients with CKD utilizing a RAAS inhibitor, a deliberate effort to reduce serum potassium levels using an approach that allows for continuation of maximally dosed RAAS inhibitor therapy is important. Patient education and engagement in the potassium management process is important for sustained success.

To provide an overview of the association between angiotensin II receptor blocker (ARB) use and cognitive outcomes. ARBs have previously shown greater neuroprotection compared to other anti-hypertensive classes. The benefits are primarily attributed to the ARB's effect on modulating the renin-angiotensin system via inhibiting the Ang II/AT1R pathway and activating the Ang II/AT2R, Ang IV/AT4R, and Ang-(1-7)/MasR pathways. These interactions are associated with pleiotropic neurocognitive benefits, including reduced β-amyloid accumulation and abnormal hyperphosphorylation of tau, ameliorated brain hypo-fusion, reduced neuroinflammation and synaptic dysfunction, better neurotoxin clearing, and blood-brain barrier function restoration. While ACEis also inhibit AT1R, they simultaneously lower Ang II and block the Ang II/AT2R and Ang IV/AT4R pathways that counterbalance the potential benefits. ARBs may be considered an adjunctive approach for neuroprotection. This preliminary evidence, coupled with their underlying mechanistic pathways, emphasizes the need for future long-term randomized trials to yield more definitive results.

Female sex hormones have systemic effects unrelated to their reproductive function. We describe experiences of different research groups and our own, on aspects related to the importance of female sex hormones on blood pressure (BP) regulation and salt-sensitivity-mediated BP response and salt sensitivity without alterations in BP, as well as renal sodium handling and interactions with the immune system. Changes in sodium intake in normotensive premenopausal women cause more BP variations than in men. After menopause, women often develop arterial hypertension (HT) with a profile of sodium sensitivity. Besides, experimental results have shown that in adult rat models resembling the postmenopausal hormonal state induced by ovariectomy, controlling BP is not enough to avoid renal and other tissue infiltration with immune cells, which does not occur when sodium intake is low or normal. Therefore, excess sodium promotes an inflammatory state with the involvement of immune cells. The evidence of activation of adaptive immunity, besides changes in T cell subpopulations, includes changes in sodium transporters and receptors. More studies are needed to evaluate the particular sodium sensitivity of women and its meaning. Changes in lifestyle and sodium intake reduction are the main therapeutic steps. However, to face the actual burden of salt-sensitive HT in postmenopausal women and its associated inflammatory/immune changes, it seems reasonable to work on immune cell activity by considering the peripheral blood mononuclear cell phenotypes of molecules and transport proteins related to sodium handle, both to screen for and treat cell activation.