Baroreceptor Stimulation for Resistant Hypertension

Yoruk, Ayhan; Bisognano, John D.; Gassler, John P.

doi:10.1093/ajh/hpw074

Cited by 13 publications

(10 citation statements)

References 19 publications

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“…It has been demonstrated that patients with hypertension develop vascular injury in the early course of the disease. Furthermore, vascular endothelial cell injury and dysfunction are important signs of hypertension and may even occur prior to the onset of hypertension ( 36 ). miRNAs serve important roles in endothelial cell injury and dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of microRNA‑506‑3p aggravates the injury of vascular endothelial cells in patients with hypertension by downregulating Beclin1 expression

Hao

Chong

et al. 2018

Exp Ther Med

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The aim of the present study was to measure the expression of microRNA (miRNA)-506-3p in the peripheral blood of patients with hypertension and to determine the biological functions and mechanisms of action of miR-506-3p. A total of 61 patients with primary hypertension were included in the present study. Peripheral blood was collected from all patients, as well as 31 healthy subjects who were included in a control group. The expression of miR-506-3p in peripheral blood was determined by reverse transcription-quantitative polymerase chain reaction. Human umbilical vein endothelial cells (HUVECs) were transfected with miR-506-3p mimics or miR-506-3p inhibitor. The proliferation and migration of HUVECs were determined using cell-counting kit 8 and Transwell assays, respectively. The cell cycle and apoptosis of HUVECs were detected by flow cytometry. The expression of Beclin1 (BECN1) protein, a potential target of miR-506-3p, was measured using western blotting. A dual-luciferase reporter assay was performed to determine the interaction between BECN1 and miR-506-3p. It was demonstrated that miR-506-3p expression in the peripheral blood of patients with patients was upregulated and dependent on the severity of hypertension. miR-506-3p overexpression inhibited the proliferation and migration of HUVECs. In addition, miR-506-3p inhibited the transition from the G1 phase to the S-phase in HUVECs. Overexpression of miR-506-3p promoted the apoptosis of HUVECs. Notably, miR-506-3p downregulated the expression of BECN1 by directly binding to its 3′-untranslated region. The present study demonstrated that miR-506-3p expression is elevated in the peripheral blood of patients with hypertension and is associated with the severity of hypertension. By downregulating BECN1 expression, miR-506-3p aggravates injury in vascular endothelial cells by inhibiting the proliferation and migration of HUVECs, as well as promoting their apoptosis.

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Section: Discussionmentioning

confidence: 99%

Overexpression of microRNA‑506‑3p aggravates the injury of vascular endothelial cells in patients with hypertension by downregulating Beclin1 expression

Hao

Chong

et al. 2018

Exp Ther Med

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“… 3 Carotid baroreceptor stimulation has been shown to exert marked blood pressure lowering effects which are mediated by the sympathoinhibitory properties of the procedure capable to substantially reduce (average reduction 30%–40%) muscle sympathetic nerve traffic. 46 Of special interest is the observation that the procedure when employed in congestive heart failure, i.e., a clinical condition characterized by a massive sympathetic activation, 47 may trigger profound sympathoinhibitory effects with a significant improvement in the clinical severity of the disease, as assessed by the New York Heart Association (NYHA) functional class. 48 …”

Section: Sns Responses To Renal Denervation and Carotid Baroreceptor Stimulationmentioning

confidence: 99%

The Sympathetic Nervous System in Hypertension: Roadmap Update of a Long Journey

Grassi

2021

American Journal of Hypertension

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The present paper will provide an update on the role of sympathetic neural factors in the development and progression of essential hypertension by reviewing data collected in the past 10 years. This will be done by discussing the results of the published studies in which sympathetic neural function in essential hypertension and related disease has been investigated via sophisticated and highly sensitive techniques, such as microneurographic recording of sympathetic nerve traffic and regional norepinephrine spillover. First, the relevance of the pathophysiological background of the neurogenic alterations will be discussed. It will be then examined the behavior of the sympathetic neural function in specific clinical phenotypes, such as resistant hypertension, pseudo-resistant hypertension and hypertensive states displaying elevated resting heart values. This will be followed by a discussion of the main results of the meta-analytic studies examining the behavior of sympathetic nerve traffic in essential hypertension, obesity, metabolic syndrome and chronic renal failure. The sympathetic effects of renal denervation and carotid baroreceptor stimulation as well as the possible involvement of sympathetic neural factors in the determination of the so-called “residual risk” of the treated hypertensive patients will be finally discussed.

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“…Even if there are not yet important studies and clear protocols, baroreflex activation therapy (BAT) could become a promising option [46] in the treatment of RH. Particularly interesting for CKD patients is that BAT was not only shown to decrease office BP values in small prospective trials on CKD non-dialysis and dialysis patients [47, 48], but also to have renoprotective effects by significantly reducing proteinuria and improving eGFR [47].…”

Section: Haemorrhagic Strokementioning

confidence: 99%

Primary Prevention of Stroke in Chronic Kidney Disease Patients: A Scientific Update

Bîlha¹,

Burlacu²,

Siriopol³

et al. 2018

Cerebrovasc Dis

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Background: Although chronic kidney disease (CKD) is an independent risk factor for stroke, official recommendations for the primary prevention of stroke in CKD are generally lacking. Summary: We searched PubMed and ISI Web of Science for randomised controlled trials, observational studies, reviews, meta-analyses and guidelines referring to measures of stroke prevention or to the treatment of stroke-associated risk factors (cardiovascular disease in general and atrial fibrillation (AF), arterial hypertension or carotid artery disease in particular) among the CKD population. The use of oral anticoagulation in AF appears safe in non-end stage CKD, but it should be individualized and preferably based on thromboembolic and bleeding stratification algorithms. Non-vitamin K antagonist oral anticoagulants with definite dose adjustment are generally preferred over vitamin K antagonists in mild and moderate CKD and their indications have started being extended to severe CKD and dialysis also. Aspirin, but not clopidogrel, has limited indications for reducing the risk for atherothrombotic events in CKD due to its increased bleeding risk. Carotid endarterectomy has shown promising results for stroke risk reduction in CKD patients with high-grade symptomatic carotid stenosis. The medical treatment of arterial hypertension in CKD often fails to efficiently lower blood pressure values, but recent data regarding the use of interventional procedures such as renal denervation, baroreflex activation therapy or renal artery stenting are encouraging. Key Messages: In the absence of clear guidelines and protocols, primary prevention of stroke in CKD patients remains a subtle art in the hands of the clinicians. Nevertheless, refraining CKD patients from standard therapies often worsens their prognosis.

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Baroreceptor Stimulation for Resistant Hypertension

Cited by 13 publications

References 19 publications

Overexpression of microRNA‑506‑3p aggravates the injury of vascular endothelial cells in patients with hypertension by downregulating Beclin1 expression

Overexpression of microRNA‑506‑3p aggravates the injury of vascular endothelial cells in patients with hypertension by downregulating Beclin1 expression

The Sympathetic Nervous System in Hypertension: Roadmap Update of a Long Journey

Primary Prevention of Stroke in Chronic Kidney Disease Patients: A Scientific Update

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