Cardiac Remodeling in Hypertension: Clinical Impact on Brain, Heart,
                    and Kidney Function

Mavrogeni, Sophie; Piaditis, George; Bacopoulou, Flora; Chrousos, George P.

doi:10.1055/a-1793-6134

Cited by 7 publications

(7 citation statements)

References 70 publications

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“…Given that hypertension itself may cause cardiac hypertrophy and increase the risk of angina and myocardial infarction ( Mavrogeni et al, 2022 ). This study was designed to observe the relationship of salt vascular and heart function.…”

Section: Resultsmentioning

confidence: 99%

Capsaicin pretreatment attenuates salt-sensitive hypertension by alleviating AMPK/Akt/Nrf2 pathway in hypothalamic paraventricular nucleus

Jia,

Yang,

Jia

et al. 2024

Front. Neurosci.

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BackgroundLong term hypertension seriously promotes target organ damage in the brain and heart, and has increasingly become serious public health problem worldwide. The anti-hypertensive effects of capsaicin has been reported, however, the role and mechanism of capsaicin within the brain on salt-induced hypertension have yet to be elucidated. This study aimed to verify the hypothesis that capsaicin attenuates salt-induced hypertension via the AMPK/Akt/Nrf2 pathway in hypothalamic paraventricular nucleus (PVN).MethodsDahl salt-sensitive (Dahl S) rats were used as animal model for the present study. Rats were randomly divided into four groups based on their dietary regimen (0.3% normal salt diet and 8% high salt diet) and treatment methods (infusion of vehicle or capsaicin in the PVN). Capsaicin was chronically administered in the PVN throughout the animal experiment phase of the study that lasted 6 weeks.ResultsOur results demonstrated that PVN pretreatment with capsaicin can slow down raise of the blood pressure elevation and heart rate (HR) of Dahl S hypertensive rats given high salt diet. Interestingly, the cardiac hypertrophy was significantly improved. Furthermore, PVN pretreatment with capsaicin induced decrease in the expression of mRNA expression of NADPH oxidase-2 (NOX2), inducible nitric oxide synthase (iNOS), NOX4, p-IKKβ and proinflammatory cytokines and increase in number of positive cell level for Nrf2 and HO-1 in the PVN of Dahl S hypertensive rats. Additionally, the protein expressions of phosphatidylinositol 3-kinase (p-PI3K) and phosphorylated protein kinase-B (p-AKT) were decreased, phosphorylated adenosine monophosphate-activated protein kinase (p-AMPK) were increased after the PVN pretreatment with capsaicin.ConclusionCapsaicin pretreatment attenuates salt-sensitive hypertension by alleviating AMPK/Akt/iNOS pathway in the PVN.

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Section: Resultsmentioning

confidence: 99%

Capsaicin pretreatment attenuates salt-sensitive hypertension by alleviating AMPK/Akt/Nrf2 pathway in hypothalamic paraventricular nucleus

Jia,

Yang,

Jia

et al. 2024

Front. Neurosci.

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“…Taken together, pathogenesis of PAH, as with essential HTN, is influenced by genetic, epigenetic, and environmental factors. Arterial hypertension is a common causative factor of vascular as well as cardiac remodeling and dysfunction [ 33 , 129 ]. Given that NLRP3 inflammasome is a key driver of vascular disease [ 130 ] and heart failure [ 131 ], it appears that enhanced NLRP3 signaling via Cx43 hemichannels may be implicated in pulmonary artery remodeling and endothelial, as well as RV, dysfunction.…”

Section: Factors and Mechanisms Involved In The Occurrence Of Cardiac...mentioning

confidence: 99%

“…According to a statement of the recent ESC 2023 congress, the effective treatment of PAH and arrhythmias are challenges in cardiac care. It seems necessary to comprehensively investigate the inter-organ and inter-cellular communication in PAH-induced RV failure and cardiac arrhythmias in patients and animal models [ 32 , 33 ].…”

Section: Introductionmentioning

confidence: 99%

Connexin43, A Promising Target to Reduce Cardiac Arrhythmia Burden in Pulmonary Arterial Hypertension

Sykora,

Szeiffova Bacova,

Andelova

et al. 2024

IJMS

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While essential hypertension (HTN) is very prevalent, pulmonary arterial hypertension (PAH) is very rare in the general population. However, due to progressive heart failure, prognoses and survival rates are much worse in PAH. Patients with PAH are at a higher risk of developing supraventricular arrhythmias and malignant ventricular arrhythmias. The latter underlie sudden cardiac death regardless of the mechanical cardiac dysfunction. Systemic chronic inflammation and oxidative stress are causal factors that increase the risk of the occurrence of cardiac arrhythmias in hypertension. These stressful factors contribute to endothelial dysfunction and arterial pressure overload, resulting in the development of cardiac pro-arrhythmic conditions, including myocardial structural, ion channel and connexin43 (Cx43) channel remodeling and their dysfunction. Myocardial fibrosis appears to be a crucial proarrhythmic substrate linked with myocardial electrical instability due to the downregulation and abnormal topology of electrical coupling protein Cx43. Furthermore, these conditions promote ventricular mechanical dysfunction and heart failure. The treatment algorithm in HTN is superior to PAH, likely due to the paucity of comprehensive pathomechanisms and causal factors for a multitargeted approach in PAH. The intention of this review is to provide information regarding the role of Cx43 in the development of cardiac arrhythmias in hypertensive heart disease. Furthermore, information on the progress of therapy in terms of its cardioprotective and potentially antiarrhythmic effects is included. Specifically, the benefits of sodium glucose co-transporter inhibitors (SGLT2i), as well as sotatercept, pirfenidone, ranolazine, nintedanib, mirabegron and melatonin are discussed. Discovering novel therapeutic and antiarrhythmic strategies may be challenging for further research. Undoubtedly, such research should include protection of the heart from inflammation and oxidative stress, as these are primary pro-arrhythmic factors that jeopardize cardiac Cx43 homeostasis, the integrity of intercalated disk and extracellular matrix, and, thereby, heart function.

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“…Given that hypertension itself may cause cardiac hypertrophy and increase the risk of angina and myocardial infarction. Hypertension is also related to the kidneys, which can exacerbate kidney disease (33). This study was designed to observe the relationship of salt and kidney function, vascular function, and heart function.…”

Section: Capsaicin Pretreatment Delayed Blood Pressure Elevation and ...mentioning

confidence: 99%

Capsaicin pretreatment attenuates salt-sensitive hypertension by alleviating AMPK/Akt/Nrf2 pathway in hypothalamic paraventricular nucleus

Jia,

Yang,

Jia

et al. 2024

Preprint

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Long term hypertension seriously affects target organ damage such as the brain, heart, and kidneys, and has become an increasingly serious public health problem worldwide. Capsaicin has been proven to improve blood pressure. However, whether capsaicin can reduce salt induced hypertension and the mechanism has yet to be elucidated. This study aimed to identify the AMPK/Akt/iNOS pathway in hypothalamic paraventricular nucleus (PVN) mediates capsaicin in improving the process of high salt induced hypertension. Dahl salt-sensitive (Dahl S) rats were uesed as the animal model for the present study. All rats were randomly divided into four groups based on their dietary regimen (0.3% salt diet and 8% salt diet) and treatment methods. Chronic administration capsaicin to the PVN during the process of blood pressure rise in rats. The entire process lasted for 6 weeks. Our results demonstrated that PVN pretreatment with capsaicin can slow down the blood pressure elevation and heart rate (HR) of Dahl S hypertensive rats. Interestingly, The cardiac hypertrophy was significantly improved. Furthermore, PVN pretreatment with capsaicin induced decrease in mRNA expression of NOX2, Inducible nitric oxide synthase (iNOS), NOX4 and proinfammatory cytokines and increase in positive cell level of Nrf2, p-IKKβ, iNOS and HO-1 in the PVN of Dahl S hypertensive rats. Additionally, the protein expressions of phosphorylated adenosine Monophosphate-activated protein kinase (p-AMPK), the phosphatidylinositol 3-kinase (p-PI3K) and phosphorylated protein kinase-B (p-AKT) were attenuated after PVN pretreatment with capsaicin. Capsaicin pretreatment attenuates salt-sensitive hypertension by alleviating AMPK/Akt/iNOS pathway in the PVN.

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Cardiac Remodeling in Hypertension: Clinical Impact on Brain, Heart, and Kidney Function

Cited by 7 publications

References 70 publications

Capsaicin pretreatment attenuates salt-sensitive hypertension by alleviating AMPK/Akt/Nrf2 pathway in hypothalamic paraventricular nucleus

Capsaicin pretreatment attenuates salt-sensitive hypertension by alleviating AMPK/Akt/Nrf2 pathway in hypothalamic paraventricular nucleus

Connexin43, A Promising Target to Reduce Cardiac Arrhythmia Burden in Pulmonary Arterial Hypertension

Capsaicin pretreatment attenuates salt-sensitive hypertension by alleviating AMPK/Akt/Nrf2 pathway in hypothalamic paraventricular nucleus

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