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Coronavirus disease-2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has affected more than seven million people worldwide, contributing to 0.4 million deaths as of June 2020. The fact that the virus uses angiotensin-converting enzyme (ACE)-2 as the cell entry receptor and that hypertension as well as cardiovascular disorders frequently coexist with COVID-19 have generated considerable discussion on the management of patients with hypertension. In addition, the COVID-19 pandemic necessitates the development of and adaptation to a “New Normal” lifestyle, which will have a profound impact not only on communicable diseases but also on noncommunicable diseases, including hypertension. Summarizing what is known and what requires further investigation in this field may help to address the challenges we face. In the present review, we critically evaluate the existing evidence for the epidemiological association between COVID-19 and hypertension. We also summarize the current knowledge regarding the pathophysiology of SARS-CoV-2 infection with an emphasis on ACE2, the cardiovascular system, and the kidney. Finally, we review evidence on the use of antihypertensive medication, namely, ACE inhibitors and angiotensin receptor blockers, in patients with COVID-19.

In mice, aldosterone administration was shown to induce oxidative stress and inflammation through vascular endothelial cells in the brain, which could be prevented by spironolactone [14]. Aldo aldosterone, BP blood pressure, CKD chronic kidney disease Compliance with ethical standards Conflict of interest The authors declare no competing interests. Association of aldosterone and blood pressure with the risk for cardiovascular events after treatments in primary aldosteronism. Association of achieved blood pressure after treatment for primary aldosteronism with long-term kidney function.

Animal studies found that irisin administration led to a significant reduction in BP in both Zucker diabetic fatty rats and spontaneously hypertensive rats, accompanied by improvements in renal sodium retention, arterial endothelial dysfunction, and oxidative stress within the paraventricular nucleus [5–7]. [...]given the conflicting results of previous clinical studies, it is possible that the clinical significance of circulating irisin levels varies among disease types. [...]evidence is needed to clarify these uncertainties, which would enhance our understanding of the mechanisms underlying hypertension and facilitate the development of novel anti-hypertensive agents. Circulating irisin level in chronic kidney disease patients: a systematic review and meta-analysis.

Pathological activation of kidney angiotensin II (Ang II) type 1 receptor (AT1R) signaling stimulates tubular sodium transporters, including epithelial sodium channels, to increase sodium reabsorption and blood pressure. During a search for a means to functionally and selectively modulate AT1R signaling, a molecule directly interacting with the carboxyl-terminal cytoplasmic domain of AT1R was identified and named AT1R-associated protein (ATRAP/Agtrap). We showed that ATRAP promotes constitutive AT1R internalization to inhibit pathological AT1R activation in response to certain stimuli. In the kidney, ATRAP is abundantly distributed in epithelial cells along the proximal and distal tubules. Results from genetically engineered mice with modified ATRAP expression show that ATRAP plays a key role in the regulation of renal sodium handling and the modulation of blood pressure in response to pathological stimuli and further suggest that the function of kidney tubule ATRAP may be different between distal tubules and proximal tubules, implying that ATRAP is a target of interest in hypertension.

Tumor necrosis factor (TNF)-α is a potent mediator of inflammation and is involved in the pathophysiology of chronic kidney disease (CKD). However, the effects of TNF-α inhibition on the progression of kidney fibrosis have not been fully elucidated. We examined the effects of TNF-α inhibition by etanercept (ETN) on kidney inflammation and fibrosis in mice with aristolochic acid (AA) nephropathy as a model of kidney fibrosis. C57BL/6 J mice were administered AA for 4 weeks, followed by a 4-week remodeling period. The mice exhibited kidney fibrosis, functional decline, and albuminuria concomitant with increases in renal mRNA expression of inflammation- and fibrosis-related genes. The 8-week ETN treatment partially but significantly attenuated kidney fibrosis and ameliorated albuminuria without affecting kidney function. These findings were accompanied by significant suppression of interleukin (IL)-1β, IL-6, and collagen types I and III mRNA expression. Moreover, ETN tended to reduce the AA-induced increase in interstitial TUNEL-positive cells with a significant reduction in Bax mRNA expression. Renal phosphorylated p38 MAPK was significantly upregulated by AA but was normalized by ETN. These findings indicate a substantial role for the TNF-α pathway in the pathogenesis of kidney fibrosis and suggest that TNF-α inhibition could become an adjunct therapeutic strategy for CKD with fibrosis.

[...]the study population included not only those with frailty but also the robust oldest old, with a blood pressure of 160 mmHg. [...]lowering the blood pressure of the frail oldest old with antihypertensive treatment might lead to the shortening of their life expectancy, akin to the observed correlation between a decrease in blood pressure and life expectancy in the frail population. [...]future studies are warranted to determine whether drug interventions or conservative treatments, such as salt restriction, should be selected (Fig. 1). [...]an increase in dBp is also correlated with the risk of mortality. [...]treatment interventions should be carefully selected based on the condition of each individual. In particular, the unaware hypertension group did not receive any antihypertensive treatment. [...]caution should be exercised when implementing an antihypertensive intervention based on the sBp in the oldest-old population, especially those with frailty, in contrast to the robust population observed in the HYVET study.

Purpose of ReviewThe renin-angiotensin-aldosterone system (RAAS) plays important roles in regulating blood pressure and body fluid, which contributes to the pathophysiology of hypertension and cardiovascular/renal diseases. However, accumulating evidence has further revealed the complexity of this signal transduction system, including direct interactions with other receptors and proteins. This review focuses on recent research advances in RAAS with an emphasis on its receptors.Recent FindingsBoth systemically and locally produced angiotensin II (Ang II) bind to Ang II type 1 receptor (AT1R) and elicit strong biological functions. Recent studies have shown that Ang II–induced activation of Ang II type 2 receptor (AT2R) elicits the opposite functions to those of AT1R. However, accumulating evidence has now expanded the components of RAAS, including (pro)renin receptor, angiotensin-converting enzyme 2, angiotensin 1–7, and Mas receptor. In addition, the signal transductions of AT1R and AT2R are regulated by not only Ang II but also its receptor-associated proteins such as AT1R-associated protein and AT2R-interacting protein. Recent studies have indicated that inappropriate activation of local mineralocorticoid receptor contributes to cardiovascular and renal tissue injuries through aldosterone-dependent and -independent mechanisms.SummarySince the mechanisms of RAAS signal transduction still remain to be elucidated, further investigations are necessary to explore novel molecular mechanisms of the RAAS, which will provide alternative therapeutic agents other than existing RAAS blockers.

Numerous studies have examined the association between each of these categories and cardiovascular disease (CVD) risk, and have shown that each subtype of hypertension has different characteristics [2, 3]. [...]it is important to determine the risk of outcome for each hypertension subtype. In this study, subjects are classified into four groups (IDH, ISH, SDH, and normotensive group) based on their baseline blood pressure (BP) values and the relationship between TyG index and CKD development is analyzed for each hypertension subtype. BP blood pressure, CKD chronic kidney disease, DBP diastolic blood pressure, IDH isolated diastolic hypertension, ISH isolated systolic hypertension, SBP systolic blood pressure, SDH systolic-diastolic hypertension, TyG triglyceride-glucose The association between TyG index and CKD have also been recently reported by others [5]. Recently, selective PPARα modulator “Pemafibrate'', which is excreted by bile, has been released and can now be used in patients with severe renal function decline, and its use in CKD patients is attracting attention [12]. [...]studies are necessary to verify whether improving TyG index with these drugs suppresses the onset and progression of CKD.