Sympathetic Nervous System Modulation of Inflammation and Remodeling in the Hypertensive Heart

Levick, Scott P.; Murray, David B.; Janicki, Joseph S.; Brower, Gregory L.

doi:10.1161/hypertensionaha.109.142042

Cited by 125 publications

(73 citation statements)

References 33 publications

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“…The effect of M40 on attenuating cardiac remodeling was shown by cardiac morphology results in the present study. It is well known that sympathetic overactivity during HF is responsible for cardiac remodeling [27]. M40 may enhance vagal activity through blocking the inhibition effect from sympathetic nerve, and vagal activity further ameliorates cardiac remodeling by counteracting sympathetic activity.…”

Section: Discussionmentioning

confidence: 99%

Effects of the Galanin Receptor Antagonist M40 on Cardiac Function and Remodeling in Rats with Heart Failure

Chen

Song

et al. 2015

Cardiovascular Therapeutics

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SUMMARYBackground: Sympathetic activation and parasympathetic withdrawal are important characteristics of heart failure. Recent studies demonstrate that galanin reduces the discharge of acetylcholine and inhibits vagal bradycardia by acting on galanin receptor type 1 (GalR1). We speculated that blocking GalR1 is beneficial for heart failure. Methods: Rats with heart failure were induced by myocardial infarction. The rats were injected intraperitoneally with galanin receptor antagonist M40 solution (30 nmol/kg) or saline for 4 weeks. Cardiac function was assessed by echocardiography and brain natriuretic peptide (BNP) in plasma. The ratio of heart weight to body weight (HW/BW), hematoxylin-eosin (HE), and Masson trichrome stain was used to evaluate cardiac remodeling. Tumor necrosis factor-a (TNF-a), interleukin 6 (IL-6) in plasma, and sarco(endo)plasmic reticulum Ca 2+ -ATPase

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Section: Discussionmentioning

confidence: 99%

Effects of the Galanin Receptor Antagonist M40 on Cardiac Function and Remodeling in Rats with Heart Failure

Chen

Song

et al. 2015

Cardiovascular Therapeutics

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“…However, a convincing and potent antifibrogenic therapeutic modality by targeting myocardial local inflammation activation is still unavailable. Recent studies have indicated that an increase of myocardial proinflammatory mediator (i.e., interleukin-6, IL-6) levels and inflammatory cells infiltration preceded the occurrence of cardiac fibrosis in response to chronic pressure overload stress (Kudo et al, 2009;Levick et al, 2009Levick et al, , 2010.…”

Section: Introductionmentioning

confidence: 99%

Oral sophocarpine protects rat heart against pressure overload-induced cardiac fibrosis

Zhao

Chu

et al. 2014

Pharmaceutical Biology

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Context: Sophocarpine, a tetracyclic quinolizidine alkaloid, is one of the most abundant active ingredients in Sophora alopecuroides Linn. (Kudouzi). Sophocarpine injection was found to have significant antiviral effects against coxsackievirus B3 and therapeutic effects for viral myocarditis in the clinic. Objective: This study assessed the effects of sophocapine on overload-induced cardiac fibrosis and investigated potential mechanisms. Materials and methods: Adult male Sprague-Dawley rats were subjected to a suprarenal abdominal aorta constriction (AC) or sham to induce sustained pressure overload. Six weeks later, rats were randomly assigned to receive sophocapine (10, 20, and 40 mg/kg, gavage) or vehicle treatment for an additional 6 weeks. Six weeks after treatment, cardiac dysfunction, cardiac coefficient, cardiac fibrosis, hydroxyproline concentration, and inflammation mediators were examined. Results: When compared with the model group, the left ventricular weight/body weight decreased by 25.4% and 39.0% in 20 and 40 mg/kg sophocarpine groups, respectively. The beneficial effects were associated with amelioration of left ventricular systolic pressure (LVSP) and left ventricular enddiastolic pressure (LVEDP). Moreover, pressure overload-induced cardiac fibrosis was attenuated in sophocarpine treated groups. Importantly, sophocarpine (20 and 40 mg/kg) decreased pro-inflammatory cytokine levels (IL-6, 14.6% and 18.5%; IL-1b, 23.1% and 32.6%), collagen content (27.7% and 50.1%), as well as matrix metalloproteinases-2, 9 (MMP-2, 9) expression (MMP-2, 11.8% and 18.5%; MMP-9, 16.2% and 21.1%). Sophocarpine (40 mg/kg) inhibited IkB-a phosphorylation (19.0%). Conclusion: These findings indicated that sophocarpine potentially had antifibrotic effects. The mechanism might be due to modulation of the balance between pro-inflammatory cytokine expression and collagen content level as well as MMPs expression via the NF-kB signaling pathway.

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“…Recent studies have shown that basic inflammatory biomarkers, such as C-reactive protein, are involved in mechanisms that lead to hypertension (18). Chronic activation of sympathetic nervous system is a key component in the development of hypertension (19). Several studies have suggested a relationship between the imbalance of the autonomic nervous system and the activation of the inflammatory system (20).…”

Section: Introductionmentioning

confidence: 99%

Inflammation is related to unbalanced cardiac autonomic functions in hypertension: an observational study

Çelik¹,

Koç²,

Kadı³

et al. 2012

Anadolu Kardiyol Derg

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Objective: Inflammation plays a role both in the mechanisms leading to hypertension alone and in the mechanisms leading to atherosclerosis with hypertension. Previous studies have shown the relationship between the autonomic functions and inflammatory system activation. The aim of the study was to evaluate the relationship between inflammation and cardiac autonomic functions in hypertensive patients. Methods: One hundred twenty one hypertensive patients (mean age 59±11 years, 60 male) and 34 healthy volunteers (mean age 58±11 years, 18 male) were included in the present cross-sectional observational study. The 24-hour ambulatory electrocardiogram recordings were taken using Pathfinder Software. The heart rate variability (HRV) analysis was performed using time domain parameters using the same software. Heart rate turbulence (HRT) parameters, turbulence onset and turbulence slope were calculated with HRT software. Statistical analysis was performed using unpaired t-test or Mann-Whitney U test, one-way ANOVA or Kruskal-Wallis analysis of variance, Chi-square test, and Spearman rank order correlation analysis. The association of hypertension with high sensitivity C-reactive protein (hs-CRP), HRV and HRT was analyzed after adjustment for confounding variables as age and creatinine levels. Results: The mean hs-CRP was higher, HRV was slightly reduced while HRT was markedly blunted in hypertensive patients in comparison with control group [SDNN; 132±28 vs. 112±34 msec, RMSSD;[27][28][29][30][31][32][33][34][35] msec, TO; -2.80±2.15 vs. -0.96±2.36%, TS; 7.56 (5.24-10.60) vs. 4.65 (2.44-7.26) msec/RR, p<0.01 for all]. All of the HRV and HRT parameters were more deteriorated in the highest tertile hs-CRP group [SDNN; 93±34 msec, RMSSD; 17 (13-22) msec, TO; 0.03±2.22%, TS; 2.43 (1.84-3.89) msec/RR, p<0.05 for all]. There were correlations between hs-CRP and HRV and HRT parameters (SDNN; r=-0.690, RMSSD; r=-0.277, TS; r:-0.417, TO; r=0.267, p<0.05 for all). Conclusion: There is an inflammatory process in hypertensive patients and inflammation is related with unbalanced cardiac autonomic functions. (Anadolu Kardiyol Derg 2012; 12: 233-40) Key words: Hypertension, inflammation, autonomic nervous system, atherosclerosis, heart rate variability, heart rate turbulence 233 ÖZET Amaç: Enflamasyonun, hem hipertansiyona sebep olan mekanizmalarda, hem de hipertansiyonla birlikte ateroskleroza sebep olan mekanizmalar içerisinde role sahip olduğu bilinmektedir. Birçok çalışmada otonom sinir sistemi ile enflamatuvar sistem aktivasyonunun ilişkisi gösterilmiş-tir. Çalışmanın amacı hipertansif hastalarda enflamasyon ile kardiyak otonomik fonksiyonlar arasındaki ilişkiyi değerlendirmektir. Yöntemler: Hipertansiyon tanısı almış 121 hasta (ortalama yaş 59±11 yıl, 60 erkek) ile 34 sağlıklı gönüllü (ortalama yaş 58±11 yıl, 18 erkek) eninekesitli gözlemsel çalışmaya alındı. Tüm katılımcılardan 24 saatlik ambulatuvar elektrokardiyogram kayıtları alınarak analizleri Pathfinder programı ile yapıldı. Kalp hızı değişkenliğinin (KHD) zaman b...

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Sympathetic Nervous System Modulation of Inflammation and Remodeling in the Hypertensive Heart

Cited by 125 publications

References 33 publications

Effects of the Galanin Receptor Antagonist M40 on Cardiac Function and Remodeling in Rats with Heart Failure

Effects of the Galanin Receptor Antagonist M40 on Cardiac Function and Remodeling in Rats with Heart Failure

Oral sophocarpine protects rat heart against pressure overload-induced cardiac fibrosis

Inflammation is related to unbalanced cardiac autonomic functions in hypertension: an observational study

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