Attenuated beta-adrenergic response to stress and increased anticipation and perception of social threat in women high on perceived criticism

2021 ◽  
pp. 105421
Author(s):  
Matias M. Pulopulos ◽  
Chelsea Boccagno ◽  
Rudi De Raedt ◽  
Jill M. Hooley
Keyword(s):  
Social Threat ◽  
Beta Adrenergic ◽  
Adrenergic Response ◽  
Response To Stress ◽  
Perceived Criticism

Modulation of beta-adrenergic response in rat brain astrocytes by serum and hormones

1985 ◽  
Vol 122 (1) ◽  
pp. 73-80 ◽  
Author(s):  
Doris K. Wu ◽  
Richard S. Morrison ◽  
Jean de Vellis
Keyword(s):  
Rat Brain ◽  
Beta Adrenergic ◽  
Adrenergic Response

PDK-1 Plays Essential Roles in the Regulation of Cell Size, Beta-adrenergic Response and Cell Survival in the Heart

2006 ◽  
Vol 12 (8) ◽  
pp. S159
Author(s):  
Kaoru Ito ◽  
Hiroshi Akazawa ◽  
Masaji Tamagawa ◽  
Norio Suda ◽  
Wataru Ogawa ◽  
...  
Keyword(s):  
Cell Survival ◽  
Cell Size ◽  
Beta Adrenergic ◽  
Adrenergic Response

scholarly journals Beta-Adrenergic Response in Human HCM Myocardium: Effects of Ranolazine

2014 ◽  
Vol 106 (2) ◽  
pp. 347a
Author(s):  
Cecilia Ferrantini ◽  
Raffaele Coppini ◽  
Benedetta Tosi ◽  
Josè Manuel Pioner ◽  
Laura Sartiani ◽  
...  
Keyword(s):  
Beta Adrenergic ◽  
Adrenergic Response

Membrane-delimited stimulation of heart cell calcium current by beta-adrenergic signal-transducing Gs protein

1990 ◽  
Vol 259 (1) ◽  
pp. H264-H267 ◽  
Author(s):  
S. Pelzer ◽  
Y. M. Shuba ◽  
T. Asai ◽  
J. Codina ◽  
L. Birnbaumer ◽  
...  
Keyword(s):  
Calcium Current ◽  
Receptor Activation ◽  
Heart Cell ◽  
Ca Channels ◽  
Beta Adrenergic ◽  
Physiological Regulation ◽  
Beta Receptor ◽  
Adrenergic Response ◽  
Gs Protein ◽  
Stimulation Of

A severalfold increase in calcium current (ICa) is a signal feature of the maximal beta-adrenergic response of the heart. It is generally ascribed to enhanced adenosine 3',5'-cyclic monophosphate (cAMP)-dependent phosphorylation of calcium (Ca) channels after beta-receptor activation of the guanosine nucleotide-binding (G) protein Gs, and Gs activation of the adenylyl cyclase cascade. We blocked phosphorylation pathways in guinea pig cardiomyocytes to unmask other possible ICa-stimulatory modes. In blocked cells, ICa increased by approximately 50% during 1) beta-receptor activation of Gs, 2) intracellular activation of Gs, and 3) intracellular application of preactivated Gs, We conclude that fast, membrane-delimited Gs modulation participates in the physiological regulation of cardiac ICa.

Increased cholinergic antagonism underlies impaired beta-adrenergic response in ovalbumin-sensitized guinea pigs

1993 ◽  
Vol 74 (6) ◽  
pp. 2729-2735 ◽  
Author(s):  
M. Wills-Karp ◽  
M. I. Gilmour
Keyword(s):  
Guinea Pig ◽  
Intrinsic Defect ◽  
Muscarinic Agonist ◽  
Muscarinic Agonists ◽  
Beta Adrenergic ◽  
Beta Adrenoceptor ◽  
Adrenergic Response ◽  
Cholinergic Pathway ◽  
Tracheal Tissue ◽  
And Control

The goal of this study was to determine if the hyporesponsiveness to beta-adrenoceptor stimulation observed in ovalbumin-sensitized tracheal smooth muscle is due to increased cholinergic muscarinic tone or to a defect in the beta-adrenergic cascade itself. We examined the effects of ovalbumin-sensitization on the responsiveness of guinea pig tracheae to agents that mediate relaxation at various steps in the beta-adrenergic cascade when the tracheal tissue was preconstricted with either carbachol or histamine. Ovalbumin sensitization caused significant reductions in the maximal relaxations both to the beta-adrenergic agonist isoproterenol and to prostaglandin E2 (PGE2) in guinea pig trachealis when the tracheal tissue was preconstricted with the muscarinic agonist carbachol. In contrast, sensitization had no effect on the ability of PGE2 and isoproterenol to relax histamine contractions. Preconstricting the tissues with increasing concentrations of KCl reduced the effectiveness of isoproterenol to relax equally airway tissues from both sensitized and control animals. Forskolin-induced relaxations of trachealis muscle were not altered with sensitization. When tracheal tissues were precontracted with increasing concentrations of carbachol, the effectiveness of isoproterenol and PGE2 to relax airway tissues decreased. Functional antagonism of relaxations by muscarinic agonists was enhanced in the sensitized tissues, since the concentration of carbachol necessary to reduce beta-adrenoceptor-induced relaxations to the same degree as in the control animals was a log dose lower. These results suggest that the impaired beta-adrenoceptor response in sensitized tissues is not due to an intrinsic defect in the beta-adrenergic cascade but to an enhancement of a muscarinic cholinergic pathway.

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