Acute effects of cardiac resynchronization therapy on arterial distensibility and serum norepinephrine levels in advanced heart failure

Yıldız, Mustafa; Hasdemir, Hakan; Türkkan, Ceyhan; Astarcıoğlu, Mehmet Ali; Alper, Ahmet Taha; Şahin, Alparslan; Özkan, Mehmet

doi:10.5603/cj.2013.0076

Cited by 2 publications

(2 citation statements)

References 38 publications

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“…An increasing number of experimental studies have suggested that PVN is key in the progression of HF (26). Studies have found that CRH and NE contribute to sympathoexcitation in rats with ischemia-induced HF (32,33). The results of the present study are consistent with these previous studies.…”

Section: Discussionsupporting

confidence: 92%

Interaction between interleukin-6 and angiotensin II receptor 1 in the hypothalamic paraventricular nucleus contributes to progression of heart failure

Wang

Gao

Xiao

et al. 2017

Molecular Medicine Reports

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The association between interleukin‑6 (IL‑6) and angiotensin II receptor 1 (AT1‑R) in modulating the progression of heart failure (HF) remains to be fully elucidated. The aim of the present study was to investigate the mechanism of IL‑6 and AT1‑R in a model of HF induced by surgery. Male Sprague‑Dawley rats were randomly divided into five groups, including sham surgery and vehicle groups. The animals were treated for 4 weeks via paraventricular nucleus infusion with either vehicle, losartan (LOS; 200 µg/day), IL‑6 (1 µg/day) or LOS and IL‑6 together (LOS+IL‑6). The rats with HF had higher levels of IL‑6, corticotropin‑releasing hormone (CRH) and norepinephrine (NE), and a lower level of neuronal nitric oxide synthase (nNOS), compared with the rats in the sham surgery group. Treatment with LOS attenuated the decrease in nNOS and the increases in IL‑6, CRH and NE; whereas treatment with IL‑6 facilitated the lower expression of nNOS and higher expression levels of IL‑6, CRH and NE. No differences in the expression levels of nNOS, CRH or NE were found between the LOS group and LOS+IL‑6 group. The results of the study demonstrated that IL‑6 contributed to the progression of HF via the AT1‑R pathway.

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Section: Discussionsupporting

confidence: 92%

Interaction between interleukin-6 and angiotensin II receptor 1 in the hypothalamic paraventricular nucleus contributes to progression of heart failure

Wang

Gao

Xiao

et al. 2017

Molecular Medicine Reports

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“…Because NE can bind various types of adrenergic receptors on the surface of immune cell membranes and then can induce intracellular signal transduction (upregulate the cAMP expression) when the serum NE level has risen. 50 Hence, BDE-209 enhanced serum NE levels and attenuated the content of NE in the hypothalamus by maternal transmission, generating the restraint of female offspring's sympathetic nervous system functions. In addition, the CNS will restrain the endings of the parasympathetic nerve from releasing Ach and impairing the bind with α7nAchR on the immune cell membrane when it receives the immune stimulation signal from the body by inhibiting the release of proinflammatory factors from immune cells through intracellular signaling pathway, the inflammatory response of the body is inhibited.…”

Section: Discussionmentioning

confidence: 99%

Role of autonomic nervous system in BDE‐209 maternal exposure induced immunotoxicity in female offspring

Mao,

Tang,

et al. 2024

Environmental Toxicology

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Decabrominated diphenyl ether (BDE‐209) is a typical persistent organic pollutant that can cross the placental barrier, increasing the exposure risk for offspring. Norepinephrine (NE) from nerve terminals and acetylcholine (Ach) can bind to specific receptors on immune cells, inhibit the immune function of the body then cause immunotoxicity. However, whether maternal exposure to BDE‐209 could lead to immunotoxicity in the offspring by acting on the sympathetic and parasympathetic nervous systems remains unclear. In view of this, the pregnancy and lactation rat BDE‐209 exposure model was established and the results demonstrated that pregnancy and lactation BDE‐209 exposure could induce immunotoxicity to female offspring via affecting immunopathology (hematological and biochemical parameters, organ indices, and spleen histopathological), decreasing humoral immunity (serum hemolysin, immunoglobulins, and cytokine productions), damaging cellular immunity (splenic lymphocytes and spleen cytokine productions), and restraining nonspecific immunity. Moreover, a dramatically significant correlation was observed between spleen nerve indices and immunity indices. Additionally, the mechanism revealed that maternal BDE‐209 exposure caused offspring immunotoxicity through (1) activating MHC/PKCθ/NF‐κB pathway; (2) promoting sympathetic nervous pathway, by upregulating the expression of β2AR protein, which in turn elevating cAMP, following activate PKA and phosphorylate CREB, ultimately leading to immunotoxicity;(3) activating parasympathetic nerve pathway by reducing the binding with Ach and α7nAchR, upregulating the expression of JAK2 and phosphorylating STAT3, induced immunotoxicity of female offspring.

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Acute effects of cardiac resynchronization therapy on arterial distensibility and serum norepinephrine levels in advanced heart failure

Abstract: Background: Cardiac resynchronization therapy (CRT) has become an accepted method for treating refractory heart failure (HF). (Cardiol J 2013; 20, 3: 304-309)

Cited by 2 publications

References 38 publications

Interaction between interleukin-6 and angiotensin II receptor 1 in the hypothalamic paraventricular nucleus contributes to progression of heart failure

Interaction between interleukin-6 and angiotensin II receptor 1 in the hypothalamic paraventricular nucleus contributes to progression of heart failure

Role of autonomic nervous system in BDE‐209 maternal exposure induced immunotoxicity in female offspring

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