Baroreflex dysfunction in chronic kidney disease

Kaur, Manpreet

doi:10.5527/wjn.v5.i1.53

Cited by 24 publications

(15 citation statements)

References 91 publications

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“…Interestingly, both of them are detectable during CKD and are reverted after renal transplantation. 57,58 Given that baroreceptors are located in the carotid bulb and are sensitive to deformations of the arterial wall, two components of the baroreflex arc can be identified: the vascular component (which is arterial stiffnessdependent) and the neural component. 59 Baroreflex function can be impaired in individuals with increased arterial stiffness as consequence of the alteration of the vascular component.…”

Section: Arterial Stiffening and Baroreflex Dysfunctionmentioning

confidence: 99%

“…110 Similar to the reduction of arterial stiffness, the baroreflex sensitivity is also improved after a renal transplant. 57 However, the mechanism by which renal transplantation can improve baroreflex function, as well as the relationship between baroreflex function and arterial properties, needs to be clarified. 111 Dialysis modalities can influence the alteration in arterial stiffness.…”

Section: Destiffening Strategiesmentioning

confidence: 99%

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Arterial Stiffness in the Heart Disease of CKD

Zanoli

Lentini

Briet

et al. 2019

JASN

139

107

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CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently overlooked. In this regard, several pathogenic factors, including uremic toxins (i.e., uric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine), can be involved. Their effect on the arterial wall, direct or mediated by chronic inflammation and oxidative stress, results in arterial stiffening and decreased vascular compliance. The increase in aortic stiffness results in increased cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascular cardiac ischemia. Conversely, reduced arterial stiffness has been associated with increased survival. Several approaches can be considered to reduce vascular stiffness and improve vascular function in patients with CKD. This review primarily discusses current understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce arterial stiffness in patients with CKD.

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Section: Arterial Stiffening and Baroreflex Dysfunctionmentioning

confidence: 99%

Section: Destiffening Strategiesmentioning

confidence: 99%

Arterial Stiffness in the Heart Disease of CKD

Zanoli

Lentini

Briet

et al. 2019

JASN

139

107

View full text Add to dashboard Cite

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“…75) We also conducted a prospective study of the effects of 3 months of treatment with a SGLT-2 inhibitor on BRS in patients with T2DM and showed that SGLT-2 inhibitors do not worsen BRS despite their diuretic effect. 76) A large percentage of patients with T2DM have complications of obesity, 13,22) hypertension, 13,15,33) dyslipidemia, 15,18,77) and chronic kidney disease, 78) which affect BRS, but as SGLT-2 inhibitors, unlike other antidiabetic drugs, have the effect of comprehensively ameliorating these complications, their efficacy in reducing BRS is expected. More large-scale clinical trials are required to study the effects of SGLT-2 inhibitors on BRS.…”

Section: Brs and Variability Of Blood Glucosementioning

confidence: 99%

Clinical Implications of Baroreflex Sensitivity in Type 2 Diabetes

Sakamoto

Matsutani

Kayama³

2019

Int. Heart J.

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The evaluation of baroreflex sensitivity (BRS), which maintains systemic circulatory homeostasis, is an established tool to assess cardiovascular autonomic neuropathy in type 2 diabetes mellitus (T2DM). As BRS plays an important function in blood pressure regulation, reduced BRS leads to an increase in blood pressure variability, which further leads to reduced BRS. This sequence of events becomes a vicious cycle. The major risk factors for reduced BRS are T2DM and essential hypertension, but many other risk factors have been reported to influence BRS. In recent years, reports have indicated that glycemic variability (GV), such as short-and longterm GV that are considered important risk factors for macrovascular and microvascular complications, is involved in reductions in BRS independently of blood glucose levels. In this review, we discuss reduced BRS in T2DM, its features, and the potential for its reversal.(Int Heart J 2019; 60: 241-246)

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“…Reduced baroreflex sensitivity has been reported in patients with VC and chronic kidney disease (Chesterton et al, 2005 ), which may contribute to dysfunction of the cardiovascular system and increased mortality (McIntyre, 2007 ; Kaur et al, 2016 ). Therefore, rescued baroreflex sensitivity might ameliorate the cardiovascular dysfunction and mortality with VC.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen Sulfide Facilitates the Impaired Sensitivity of Carotid Sinus Baroreflex in Rats with Vascular Calcification

Teng

Guo

et al. 2017

Front. Pharmacol.

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Arterial baroreflex is a general mechanism maintaining cardiovascular homeostasis; its sensitivity is reduced in vascular calcification (VC). Hydrogen sulfide (H2S) treatment facilitates baroreflexive sensitivity in normal and hypertensive rats. Here, we aimed to detect the effect of H2S on baroreflexive sensitivity in rats with VC. The rat VC model was induced by vitamin D3 plus nicotine for 4 weeks. The sensitivity of baroreflex was detected by perfusing the isolated carotid sinus. VC was assessed by hematoxylin and eosin (H&E) staining, Ca2+ content and alkaline phosphatase (ALP) activity. Protein levels were detected by western blot analysis. Vitamin D3 plus nicotine induced structural disorder and elevated Ca2+ content in the aortic and carotid arterial wall and increased plasma ALP activity. In the calcified aorta and carotid artery, protein levels of contractile phenotype markers of vascular smooth muscle cells (VSMCs) were downregulated and that of osteoblast-like phenotype markers and endoplasmic reticulum stress (ERS) markers were upregulated. NaHS treatment ameliorated the histologic disorder and Ca2+ content in the calcified aorta and carotid artery, inhibited the elevated plasma ALP activity, and prevented the transformation of the VSMC phenotype and activation of ERS in rats with VC. Chronic NaHS treatment prevented the impairment of the baroreflex sensitivity and acute NaHS treatment dose-dependently improved the sensitivity in rats with VC. Our results suggested that H2S could directly facilitate the impairment of baroreflex in rats with VC and ameliorate VC, which might provide new target and strategy for regulation of the baroreflex and therapy of VC.

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Baroreflex dysfunction in chronic kidney disease

Cited by 24 publications

References 91 publications

Arterial Stiffness in the Heart Disease of CKD

Arterial Stiffness in the Heart Disease of CKD

Clinical Implications of Baroreflex Sensitivity in Type 2 Diabetes

Hydrogen Sulfide Facilitates the Impaired Sensitivity of Carotid Sinus Baroreflex in Rats with Vascular Calcification

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