Molsidomine Attenuates Ventricular Electrical Remodeling and Arrhythmogenesis in Rats With Chronic β-Adrenergic Receptor Activation Through the NO/cGMP/PKG Pathway

2016 ◽  
Vol 68 (5) ◽  
pp. 342-355 ◽  
Author(s):  
Yingguang Shan ◽  
Dandan Wang ◽  
Ran Li ◽  
Congxin Huang
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Electrical Remodeling ◽  
Ventricular Electrical Remodeling

scholarly journals Mechanisms of L-Triiodothyronine-Induced Inhibition of Synaptosomal Na+-K+-ATPase Activity in Young Adult Rat Brain Cerebral Cortex

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Pradip K. Sarkar ◽  
Avijit Biswas ◽  
Arun K. Ray ◽  
Joseph V. Martin
Keyword(s):  
Cerebral Cortex ◽  
Atpase Activity ◽  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Mammalian Brain ◽  
Neuronal Membrane ◽  
Dependent Manner ◽  
Adrenergic Agonist ◽  
Adult Rat ◽  
Dose Dependent

The role of thyroid hormones (TH) in the normal functioning of adult mammalian brain is unclear. Our studies have identified synaptosomal Na+-K+-ATPase as a TH-responsive physiological parameter in adult rat cerebral cortex. L-triiodothyronine (T3) and L-thyroxine (T4) both inhibited Na+-K+-ATPase activity (but not Mg2+-ATPase activity) in similar dose-dependent fashions, while other metabolites of TH were less effective. Although both T3and theβ-adrenergic agonist isoproterenol inhibited Na+-K+-ATPase activity in cerebrocortical synaptosomes in similar ways, theβ-adrenergic receptor blocker propranolol did not counteract the effect of T3. Instead, propranolol further inhibited Na+-K+-ATPase activity in a dose-dependent manner, suggesting that the effect of T3on synaptosomal Na+-K+-ATPase activity was independent ofβ-adrenergic receptor activation. The effect of T3on synaptosomal Na+-K+-ATPase activity was inhibited by theα2-adrenergic agonist clonidine and by glutamate. Notably, both clonidine and glutamate activateGi-proteins of the membrane second messenger system, suggesting a potential mechanism for the inhibition of the effects of TH. In this paper, we provide support for a nongenomic mechanism of action of TH in a neuronal membrane-related energy-linked process for signal transduction in the adult condition.

scholarly journals Coupling of lipolysis and de novo lipogenesis in brown, beige, and white adipose tissues during chronic β3-adrenergic receptor activation

2014 ◽  
Vol 55 (11) ◽  
pp. 2276-2286 ◽  
Author(s):  
Emilio P. Mottillo ◽  
Priya Balasubramanian ◽  
Yun-Hee Lee ◽  
Changren Weng ◽  
Erin E. Kershaw ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
De Novo ◽  
Receptor Activation ◽  
De Novo Lipogenesis ◽  
Adipose Tissues

scholarly journals β2-Adrenergic receptor activation on donor cells ameliorates acute GvHD

JCI Insight ◽  
2020 ◽  
Vol 5 (12) ◽  
Author(s):  
Hemn Mohammadpour ◽  
Joseph L. Sarow ◽  
Cameron R. MacDonald ◽  
George L. Chen ◽  
Jingxin Qiu ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Acute Gvhd ◽  
Receptor Activation ◽  
Donor Cells ◽  
Β2 Adrenergic Receptor

scholarly journals Norepinephrine promotes triglyceride storage in macrophages via beta2‐adrenergic receptor activation

2021 ◽  
Vol 35 (2) ◽  
Author(s):  
Kasparas Petkevicius ◽  
Guillaume Bidault ◽  
Sam Virtue ◽  
Benjamin Jenkins ◽  
Xanthe A. M. H. Dierendonck ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Activation
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