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Separate and combined blockades of α- and β-adrenergic receptors in forearm sweating induced by adrenergic agents and exercise in the heat in young adults.

Am J Physiol Regul Integr Comp Physiol

February 2025

Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.

The assessment of adrenergic modulation of sweating as assessed via pharmacologic administration of α- and β-adrenergic receptor blockers during exercise has yielded mixed findings. However, the underlying mechanisms for this disparity remain unresolved. We investigated the effects of separate and combined blockade of α- and β-adrenergic receptors on forearm sweating induced by a 30-min moderate-intensity exercise bout ( = 17, ) and the administration of adrenergic agonists epinephrine and norepinephrine ( = 16, ) in the heat.

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Background ADRB1 (adrenergic receptor beta 1) responds to neuroendocrine stimulations, which have great implications in hypertension. GRK2 (G protein-coupled receptor kinase 2) is an essential regulator for many G protein-coupled receptors and subsequent cell signaling cascades, but its role as a regulator of ADRB1 and associated cardiac hypertrophy in hypertension remains to be elucidated. Methods and Results In this study, we found the expressions of GRK2 and ADRB1 in peripheral blood mononuclear cells were positively associated with blood pressure levels in hypertensive patients and with their expression in heart.

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Role of Kv1.3 Channels in Platelet Functions and Thrombus Formation.

Arterioscler Thromb Vasc Biol

October 2020

Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (K.L.).

Objective: Platelet activation by stimulatory factors leads to an increase in intracellular calcium concentration ([Ca]), which is essential for almost all platelet functions. Modulation of Ca influx and [Ca] in platelets has been emerging as a possible strategy for preventing and treating platelet-dependent thrombosis. Voltage-gated potassium 1.

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Valsartan impedes epinephrine-induced ICAM-4 activation on normal, sickle cell trait and sickle cell disease red blood cells.

PLoS One

January 2020

New England Sickle Cell Institute, Division of Hematology-Oncology, Neag Comprehensive Cancer Center, UCONN Health, University of Connecticut, Farmington, Connecticut, United States of America.

Abnormal red blood cell (RBC) adhesion to endothelial αvβ3 plays a crucial role in triggering vaso-occlusive episodes in sickle cell disease (SCD). It is known that epinephrine, a β-adrenergic receptor (β-AR) stimulator, increases the RBC surface density of active intercellular adhesion molecule-4 (ICAM-4) which binds to the endothelial αvβ3. It has also been demonstrated that in human embryonic kidney 293 cells, mouse cardiomyocytes, and COS-7 cell lines, the β-adrenergic and renin-angiotensin systems are interrelated and that there is a direct interaction and cross-regulation between β-AR and angiotensin II type 1 receptor (AT1R).

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Voluntary Running Suppresses Tumor Growth through Epinephrine- and IL-6-Dependent NK Cell Mobilization and Redistribution.

Cell Metab

March 2016

Centre of Inflammation and Metabolism and Centre for Physical Activity Research, Rigshospitalet, Faculty of Health Science, University of Copenhagen, DK-2100, Denmark; Department of Oncology, Copenhagen University Hospital, Herlev, DK-2730, Denmark. Electronic address:

Regular exercise reduces the risk of cancer and disease recurrence. Yet the mechanisms behind this protection remain to be elucidated. In this study, tumor-bearing mice randomized to voluntary wheel running showed over 60% reduction in tumor incidence and growth across five different tumor models.

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