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

Chen, Ao; Li, Min; Song, Lei; Zhang, Yunhe; Luo, Zhangyuan; Zhang, Wenzan; Chen, Yingmin; He, Ben

doi:10.1111/1755-5922.12144

Cited by 19 publications

(15 citation statements)

References 30 publications

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“…Galanin is involved in central cardiovascular regulation, which affects the blood pressure and the heart rate [2]. Administration of galanin into the rostral ventrolateral medulla produces a weak hypotension and tachycardia effect by reducing the sympathetic vasomotor tone in rats [3], which may be blocked by the intracerebroventricular injection of galanin antagonist M40 [4]. Recent studies suggest that galanin and its fragment play a major role in the regulation of metabolic homeostasis in cardiac muscle and galanin is an important hormone relative to diabetic heart [4].…”

Section: Introductionmentioning

confidence: 99%

“…Administration of galanin into the rostral ventrolateral medulla produces a weak hypotension and tachycardia effect by reducing the sympathetic vasomotor tone in rats [3], which may be blocked by the intracerebroventricular injection of galanin antagonist M40 [4]. Recent studies suggest that galanin and its fragment play a major role in the regulation of metabolic homeostasis in cardiac muscle and galanin is an important hormone relative to diabetic heart [4]. The endogenous galanin, acting through its central receptor, has an important attribute to glucose transporter 4 (GLUT4) regulation, leading to enhanced insulin sensitivity and glucose uptake in cardiac muscle of type 2 diabetic rats [5].…”

Section: Introductionmentioning

confidence: 99%

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Myocardial protection from ischemia/reperfusion injury by exogenous galanin fragment

et al. 2017

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Background and purpose: Galanin is a multifunctional neuropeptide with pleiotropic roles. The present study was designed to evaluate the potential effects of galanin (2-11) (G1) on functional and metabolic abnormalities in response to myocardial ischemia-reperfusion (I/R) injury. Experimental approach: Peptide G1 was synthesized by the 9-fluorenylmethoxycarbonyl (Fmoc)-based solid-phase method. The chemical structure was identified by

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Myocardial protection from ischemia/reperfusion injury by exogenous galanin fragment

et al. 2017

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“…In myocytes, galanin improved contractile performance of papillary muscles following simulated ischemia reperfusion. However, induction of MI in rats treated with the GalR antagonist M40 (30 nmol/kg IP, for four weeks), showed that M40 imparted small improvements in ejection fraction and a slightly reduced LV chamber dimension compared with MI controls, resulting in a slightly reduced heart weight to body weight ratio [199]. This was accompanied by small reductions in BNP and IL-6, but not TNF-α.…”

Section: 0 Additional Neuropeptidesmentioning

confidence: 99%

The role of neuropeptides in adverse myocardial remodeling and heart failure

Widiapradja

Chunduri

Levick

2017

Cell. Mol. Life Sci.

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In addition to traditional neurotransmitters of the sympathetic and parasympathetic nervous systems, the heart also contains numerous neuropeptides. These neuropeptides not only modulate the effects of neurotransmitters, but also have independent effects on cardiac function. While in most cases the physiological actions of these neuropeptides are well defined, their contributions to cardiac pathology are less appreciated. Some neuropeptides are cardioprotective, some promote adverse cardiac remodeling and heart failure, and in the case of others their functions are unclear. Some have both cardioprotective and adverse effects depending on the specific cardiac pathology and progression of that pathology. In this review, we briefly describe the actions of several neuropeptides on normal cardiac physiology, before describing in more detail their role in adverse cardiac remodeling and heart failure. It is our goal to bring more focus toward understanding the contribution of neuropeptides to the pathogenesis of heart failure, and to consider them as potential therapeutic targets.

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“…The experimental model of heart failure was induced by ligation of the left anterior descending coronary artery (LAD) as previously described. 17) Briefly, rats were anaesthetized with 3% pentobarbital sodium (30 mg/kg, ip) and intubated for mechanical ventilation (SAR-830, CWE Inc., USA). A left thoracotomy was performed and then the LAD was exposed and ligated with a 6-0 silk suture after the pericardium was cut.…”

Section: H Eart Failure (Hf) Is a Clinical Syndrome Characterizedmentioning

confidence: 99%

Low-Level Vagus Nerve Stimulation Reverses Cardiac Dysfunction and Subcellular Calcium Handling in Rats With Post-Myocardial Infarction Heart Failure

et al. 2016

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SummaryVagus nerve stimulation (VNS), targeting the imbalanced autonomic nervous system, is a promising therapeutic approach for chronic heart failure (HF). Moreover, calcium cycling is an important part of cardiac excitation-contraction coupling (ECC), which also participates in the antiarrhythmic effects of VNS. We hypothesized that low-level VNS (LL-VNS) could improve cardiac function by regulation of intracellular calcium handling properties. The experimental HF model was established by ligation of the left anterior descending coronary artery (LAD). Thirty-two male Sprague-Dawley rats were divided into 3 groups as follows; control group (sham operated without coronary ligation, n = 10), HF-VNS group (HF rats with VNS, n = 12), and HF-SS group (HF rats with sham nerve stimulation, n = 10). After 8 weeks of treatment, LL-VNS significantly improved left ventricular ejection fraction (LVEF) and attenuated myocardial interstitial fibrosis in the HF-VNS group compared with the HF-SS group. Elevated plasma norepinephrine and dopamine, but not epinephrine, were partially reduced by LL-VNS. Additionally, LL-VNS restored the protein and mRNA levels of sarcoplasmic reticulum Ca 2+ ATPase (SERCA2a), Na + -Ca 2+ exchanger 1 (NCX1), and phospholamban (PLB) whereas the expression of ryanodine receptor 2 (RyR2) as well as mRNA level was unaffected. Thus, our study results suggest that the improvement of cardiac performance by LL-VNS is accompanied by the reversal of dysfunctional calcium handling properties including SERCA2a, NCX1, and PLB which may be a potential molecular mechanism of VNS for HF. (Int Heart J 2016; 57: 350-355)

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

Cited by 19 publications

References 30 publications

Myocardial protection from ischemia/reperfusion injury by exogenous galanin fragment

Myocardial protection from ischemia/reperfusion injury by exogenous galanin fragment

The role of neuropeptides in adverse myocardial remodeling and heart failure

Low-Level Vagus Nerve Stimulation Reverses Cardiac Dysfunction and Subcellular Calcium Handling in Rats With Post-Myocardial Infarction Heart Failure

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