Purification of β-Adrenergic Receptors

1990 ◽  
pp. 45-75 ◽  
Author(s):  
Craig C. Malbon
Keyword(s):  
Adrenergic Receptors ◽  
Β Adrenergic Receptors

Molecular Docking and Drug Discovery in β-Adrenergic Receptors

2017 ◽  
Vol 24 (39) ◽  
Author(s):  
Santiago Vilar ◽  
Eduardo Sobarzo-Sanchez ◽  
Lourdes Santana ◽  
Eugenio Uriarte
Keyword(s):  
Molecular Docking ◽  
Drug Discovery ◽  
Adrenergic Receptors ◽  
Β Adrenergic Receptors

scholarly journals Role of β-Adrenergic Receptors and Nitric Oxide Signaling in Exercise-Mediated Cardioprotection

Physiology ◽  
2013 ◽  
Vol 28 (4) ◽  
pp. 216-224 ◽  
Author(s):  
John W. Calvert ◽  
David J. Lefer
Keyword(s):  
Nitric Oxide ◽  
Risk Factors ◽  
Adrenergic Receptors ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Signaling ◽  
Factors Associated ◽  
Cardioprotective Effects ◽  
Β Adrenergic Receptors

Exercise promotes cardioprotection in both humans and animals not only by reducing risk factors associated with cardiovascular disease but by reducing myocardial infarction and improving survival following ischemia. This article will define the role that nitric oxide and β-adrenergic receptors play in mediating the cardioprotective effects of exercise in the setting of ischemia-reperfusion injury.

Chronic Effects of Metoprolol on Myocardial β-Adrenergic Receptors in Doxorubicin-Induced Cardiac Damage in Rats

1991 ◽  
Vol 17 (4) ◽  
pp. 656-661 ◽  
Author(s):  
Naoya Fujita ◽  
Michiaki Hiroe ◽  
Yotihiko Ohta ◽  
Toshinobu Horie ◽  
Saichi Hosoda
Keyword(s):  
Adrenergic Receptors ◽  
Cardiac Damage ◽  
Chronic Effects ◽  
Β Adrenergic Receptors

α-Adrenergic receptor modulation of the intrathoracic efferent sympathetic nervous system regulating the canine heart

1989 ◽  
Vol 67 (10) ◽  
pp. 1199-1204 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Blocking Agent ◽  
Sympathetic Ganglia ◽  
Canine Heart ◽  
Receptor Modulation ◽  
Adrenergic Antagonist ◽  
Cervical Ganglia ◽  
Β Adrenergic Receptors ◽  
Stimulation Of

The augmentation of ventricular inotropism induced by electrical stimulation of acutely decentralized efferent sympathetic preganglionic axons was reduced, but still present, following administraiton of hexamethonium (10 mg/kg i.v.). While hexamethonium continued to be administered, the cardiac augmentations so induced were enhanced significantly following administration of the α-adrenergic receptor blocking agent, phentolamine myselate (1 mg/kg i.v.). Stimulation of the sympathetic efferent postganglionic axons in cardiopulmonary nerves induced cardiac augmentations that were unchanged following administration of these agents singly or together. The cardiac augmentations induced by stimulation of efferent preganglionic sympathetic axons were unchanged when phentolamine was administered alone. The augmentations of cardiac inotropism induced by efferent postganglionic sympathetic axonal stimulation were decreased following local administration of the β-adrenergic antagonist timolol into the ipsilateral stellate and middle cervical ganglia. Thereafter, these augmentations were unchanged following the subsequent intravenous administration of phentolamine. It is concluded that the activation of cardiac neurons in the stellate and middle cervical ganglia by stimulation of efferent preganglionic sympathetic axons can be modified by α-adrenergic receptors and that these effects are dependent upon β-adrenergic receptors, not nicotinic ones, in intrathoracic ganglia.Key words: α-adrenergic inotropism, sympathetic ganglia, hexamethonium, phentolamine.

Effects of thyroid state on brain development: β-Adrenergic receptors and 5′-nucleotidase activity

1980 ◽  
Vol 198 (2) ◽  
pp. 375-387 ◽  
Author(s):  
R.M. Smith ◽  
A.J. Patel ◽  
A.E. Kingsbury ◽  
A. Hunt ◽  
R. Bala´zs
Keyword(s):  
Brain Development ◽  
Adrenergic Receptors ◽  
Nucleotidase Activity ◽  
Thyroid State ◽  
Β Adrenergic Receptors

Chronic administration of sertraline, a selective serotonin uptake inhibitor, decreased the density of β-adrenergic receptors in rat frontoparietal cortex

1987 ◽  
Vol 421 (1-2) ◽  
pp. 377-381 ◽  
Author(s):  
William F. Byerley ◽  
Elizabeth J. McConnel ◽  
R. Tyler McCabe ◽  
Ted M. Dawson ◽  
Bernard I. Grosser ◽  
...  
Keyword(s):  
Adrenergic Receptors ◽  
Chronic Administration ◽  
Serotonin Uptake ◽  
Selective Serotonin ◽  
Uptake Inhibitor ◽  
Serotonin Uptake Inhibitor ◽  
Frontoparietal Cortex ◽  
Β Adrenergic Receptors

Decreased glucagon binding and glucagon-stimulated lipolysis in adipocytes from streptozotocin-diabetic rats

1989 ◽  
Vol 121 (5) ◽  
pp. 705-713 ◽  
Author(s):  
Nobuyuki Sato ◽  
Minoru Irie ◽  
Hiroshi Kajinuma ◽  
Kazuo Suzuki
Keyword(s):  
Quantitative Analysis ◽  
Cyclic Amp ◽  
Adrenergic Receptors ◽  
Marked Reduction ◽  
Diabetic Rats ◽  
Down Regulation ◽  
Streptozotocin Diabetic Rats ◽  
Β Adrenergic Receptors ◽  
Glucagon Receptors ◽  
The Relationship

Abstract. Adipocytes from streptozotocin-diabetic rats showed a markedly reduced lipolytic response to glucagon concomitant with a 90% or greater decrease in the number of glucagon receptors per cell. In contrast, β-adrenergic receptors assessed by [3H]dihydroalprenolol binding and lipolysis stimulated by isoproterenol, dibutyryl 3′5′-cyclic AMP and 3-isobutyl-1-methylxanthine were reduced by only 10–25% in diabetic rats compared with controls. Furthermore, quantitative analysis of the relationship between the amount of cell-bound glucagon and the hormone-stimulated lipolysis revealed that the function of the remaining 10% of glucagon receptors remained intact in cells from diabetic animals. These findings suggest that the lipolytic cascades, including β-adrenergic receptors, in adipocytes are not greatly impaired by diabetes, and therefore, the unresponsiveness of these cells to glucagon is mostly due to a marked reduction in the number of glucagon receptors, probably as a result of a down-regulation by postprandial hyperglucagonemia.

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