scholarly journals A reduction in SK channels contributes to increased activity of hypothalamic magnocellular neurons during heart failure

2017 ◽  
Vol 595 (20) ◽  
pp. 6429-6442 ◽  
Author(s):  
Hildebrando C. Ferreira-Neto ◽  
Vinicia C. Biancardi ◽  
Javier E. Stern
Keyword(s):  
Heart Failure ◽  
Sk Channels ◽  
Magnocellular Neurons ◽  
Increased Activity

scholarly journals Cardiac Protection of Valsartan on Juvenile Rats with Heart Failure by Inhibiting Activity of CaMKII via Attenuating Phosphorylation

2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Yao Wu ◽  
Feifei Si ◽  
Xiaojuan Ji ◽  
Kunfeng Jiang ◽  
Sijie Song ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Myocyte ◽  
Pressure Overload ◽  
The Other ◽  
Calcium Handling ◽  
Juvenile Rats ◽  
Abdominal Aortic ◽  
Calcium Handling Proteins ◽  
Increased Activity ◽  
Induce Heart Failure

Background. This study was undertaken to determine relative contributions of phosphorylation and oxidation to the increased activity of calcium/calmodulin-stimulated protein kinase II (CaMKII) in juveniles with cardiac myocyte dysfunction due to increased pressure overload. Methods. Juvenile rats underwent abdominal aortic constriction to induce heart failure. Four weeks after surgery, rats were then randomly divided into two groups: one group given valsartan (HF + Val) and the other group given placebo (HF + PBO). Simultaneously, the sham-operated rats were randomly given valsartan (Sham + Val) or placebo (Sham + PBO). After 4 weeks of treatment, Western blot analysis was employed to quantify CaMKII and relative calcium handling proteins (RyR2 and PLN) in all groups. Results. The deteriorated cardiac function was reversed by valsartan treatment. In ventricular muscle cells of group HF + PBO, Thr287 phosphorylation of CaMKII and S2808 phosphorylation of RyR2 and PLN were increased and S16 phosphorylation of PLN was decreased compared to the other groups, while Met281 oxidation was not significantly elevated. In addition, these changes in the expression of calcium handling proteins were ameliorated by valsartan administration. Conclusions. The phosphorylation of Thr286 is associated with the early activation of CaMKII rather than the oxidation of Met281.

scholarly journals Cardiopulmonary syndrome and adrenoreactivity of an organism

2016 ◽  
Vol 97 (6) ◽  
pp. 864-869 ◽  
Author(s):  
V M Gazizyanova ◽  
O V Bulashova ◽  
A A Nasybullina ◽  
Z A Shaykhutdinova ◽  
A A Podol’skaya
Keyword(s):  
Heart Failure ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Clinical Features ◽  
Clinical Manifestations ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Heart Failure Patients ◽  
Increased Activity

Aim. To study β-adrenoreactivity of the cell membrane in patients with different variants of heart failure in association with chronic obstructive pulmonary disease.Methods. 120 heart failure patients including 68 of them who suffer from concominant chronic obstructive pulmonary disease were evaluated. Assessment of clinical features of heart failure, patients’ quality of life and study of β-adrenoreactivity were performed.Results. Adrenoreactivity of an organism in heart failure and concominant chronic obstructive pulmonary disease was 2 times higher and was 55.4±18.8 U and in heart failure only it was 29.4±8.5 U. Intensification of β-adrenoreactivity was found to be proportional to worsening of clinical features of chronic heart failure in all patients that was more prominent in patients with pulmonary disease. Responders with heart failure in association with chronic obstructive pulmonary disease had higher values of β-adrenoreactivity of cell membranes more frequently.Conclusion. The results of our investigation confirm increased activity of sympathetic system in heart failure and concominant chronic obstructive pulmonary disease that worsens clinical manifestations of heart failure.

scholarly journals Expression of a Gi-coupled receptor in the heart causes impaired Ca2+ handling, myofilament injury, and dilated cardiomyopathy

2008 ◽  
Vol 294 (1) ◽  
pp. H205-H212 ◽  
Author(s):  
Diana T. McCloskey ◽  
Sally Turcato ◽  
Guan-Ying Wang ◽  
Lynne Turnbull ◽  
Bo-Qing Zhu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Matrix Metalloproteinase 2 ◽  
Human Heart Failure ◽  
Transient Time ◽  
Conditional Expression ◽  
Perfused Hearts ◽  
Camp Levels ◽  
Increased Activity ◽  
Ventricular Trabeculae

Increased signaling by Gi-coupled receptors has been implicated in dilated cardiomyopathy. To investigate the mechanisms, we used transgenic mice that develop dilated cardiomyopathy after conditional expression of a cardiac-targeted Gi-coupled receptor (Ro1). Activation of Gi signaling by the Ro1 agonist spiradoline caused decreased cellular cAMP levels and bradycardia in Langendorff-perfused hearts. However, acute termination of Ro1 signaling with the antagonist nor-binaltorphimine did not reverse the Ro1-induced contractile dysfunction, indicating that Ro1 cardiomyopathy was not due to acute effects of receptor signaling. Early after initiation of Ro1 expression, there was a 40% reduction in the abundance of the sarcoplasmic reticulum Ca2+-ATPase ( P < 0.05); thereafter, there was progressive impairment of both Ca2+ handling and force development assessed with ventricular trabeculae. Six weeks after initiation of Ro1 expression, systolic Ca2+ concentration was reduced to 0.61 ± 0.08 vs. 0.91 ± 0.07 μM for control ( n = 6–8; P < 0.05), diastolic Ca2+ concentration was elevated to 0.41 ± 0.07 vs. 0.23 ± 0.06 μM for control ( n = 6–8; P < 0.01), and the decline phase of the Ca2+ transient (time from peak to 50% decline) was slowed to 0.25 ± 0.02 s vs. 0.13 ± 0.02 s for control ( n = 6–8; P < 0.01). Early after initiation of Ro1 expression, there was a ninefold elevation of matrix metalloproteinase-2 ( P < 0.01), which is known to cause myofilament injury. Consistent with this, 6 wk after initiation of Ro1 expression, Ca2+-saturated myofilament force in skinned trabeculae was reduced to 21 ± 2 vs. 38 ± 0.1 mN/mm2 for controls ( n = 3; P < 0.01). Furthermore, electron micrographs revealed extensive myofilament damage. These findings may have implications for some forms of human heart failure in which increased activity of Gi-coupled receptors leads to impaired Ca2+ handling and myofilament injury, contributing to impaired ventricular pump function and heart failure.

scholarly journals Increased Activity of the Intracardiac Oxytocinergic System in the Development of Postinfarction Heart Failure

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Agnieszka Wsol ◽  
Kaja Kasarello ◽  
Marek Kuch ◽  
Kamila Gala ◽  
Agnieszka Cudnoch-Jedrzejewska
Keyword(s):  
Heart Failure ◽  
Mrna Expression ◽  
Protein Level ◽  
Oxytocin Receptor ◽  
Sprague Dawley ◽  
Rt Pcr ◽  
Sham Surgery ◽  
Sprague Dawley Rats ◽  
The Right ◽  
Increased Activity

Aim.The present study was designed to test the hypothesis that the development of postinfarction heart failure is associated with a change of activity of the intracardiac oxytocinergic system.Methods.Experiments were performed on male Sprague-Dawley rats subjected to myocardial infarction or sham surgery. Four weeks after the surgery, blood samples were collected and the samples of the left ventricle (LV) and right ventricle (RV) were harvested for evaluation of the mRNA expression (RT-PCR) of oxytocin (OT), oxytocin receptor (OTR), natriuretic peptides, and the level of OT and OTR protein (ELISA). The concentration of N-terminal B-type natriuretic peptide was measured to determine the presence of heart failure.Results.Plasma NT-proBNP concentration was higher in the infarcted rats. In the infarcted rats, the expression of OT mRNA and the OT protein level were higher in the RV. There were no significant differences between infarcted and noninfarcted rats in the expression of OT mRNA and in the OT protein level in the fragments of the LV. In both the left and the right ventricles, OTR mRNA expression was lower but the level of OTR protein was higher in the infarcted rats.Conclusions.In the present study, we indicate that postinfarction heart failure is associated with an increased activity of the intracardiac oxytocinergic system.

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