scholarly journals Efficacy and potency of alpha adrenergic receptor agonists at inhibiting rat hippocampal CA3 network activity

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Lorraine O'shea ◽  
Sarah Boese ◽  
Ke Xu ◽  
Brian Nelson ◽  
Brianna Goldenstein ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Network Activity ◽  
Receptor Agonists ◽  
Alpha Adrenergic Receptor ◽  
Hippocampal Ca3

Regulation of canine platelet function II. Catecholamines

1983 ◽  
Vol 245 (1) ◽  
pp. R100-R109 ◽  
Author(s):  
K. M. Meyers ◽  
L. Y. Huston ◽  
R. M. Clemmons
Keyword(s):  
Arachidonic Acid ◽  
Adrenergic Receptor ◽  
Dense Granule ◽  
Platelet Response ◽  
Receptor Agonists ◽  
Alpha Adrenergic Receptor ◽  
Acid Metabolites ◽  
Induced Aggregation ◽  
The Relationship ◽  
Platelet Shape

The action of epinephrine (E) on canine platelet aggregation is described. Although E did not induce a change in platelet shape or aggregation, potentiation of aggregation induced by the following agents was observed at physiological E concentrations (that is, less than 10 nM/1): arachidonic acid; the dense granule agonists, ADP and serotonin (5-HT); and collagen. Epinephrine-induced potentiation was in part independent of formation of arachidonic acid metabolites, and E potentiated the aggregating action of the bivalent cationophore A23187. Potentiation was inhibited by alpha-adrenergic receptor antagonists phenoxybenzamine, phentolamine, and ergotamine, and mimicked by alpha-adrenergic receptor agonists norepinephrine, clonidine, and in some cases, phenylephrine. The beta-adrenergic receptor agonists isoproterenol and dobutamine inhibited ADP-induced aggregation, and this action was presented by pretreating the platelets with propranolol and dichloroisoproterenol. An augmentation of the aggregation response of platelets to arachidonic acid was observed in blood samples withdrawn when circulating catecholamines were elevated. The physiological implication of epinephrine acting as a gain controller that alters the relationship between actuating signal and the platelet response to an agonist is discussed.

Baroreflex mechanisms buffering alpha-adrenergic agonists in conscious dogs

1987 ◽  
Vol 253 (4) ◽  
pp. H728-H736
Author(s):  
A. M. Fujii ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Adrenergic Receptor ◽  
Peripheral Resistance ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Receptor Agonists ◽  
Alpha Adrenergic Receptor

To determine the relative importance of the mechanisms utilized by the arterial baroreflex in buffering the pressor and vasoconstrictor responses to alpha-adrenergic receptor agonists, we studied responses to norepinephrine and phenylephrine in conscious dogs. The dogs were studied 2-8 wk after instrumentation with aortic catheters and aortic electromagnetic flow probes to measure arterial pressure and cardiac output. Total peripheral resistance was calculated on-line by a digital computer. The dogs were studied after beta-adrenergic receptor blockade (propranolol 1.0 mg/kg) to eliminate the complicating inotropic effects of the agonists studied. Norepinephrine (0.2 microgram/kg bolus) increased mean arterial pressure by 30 +/- 3 mmHg, total peripheral resistance by 51 +/- 4 mmHg . l-1 . min-1, and decreased heart rate by 26 +/- 3 beats/min. After arterial baroreceptor denervation, norepinephrine increased mean arterial pressure by 69 +/- 8 mmHg, total peripheral resistance by 48 +/- 6 mmHg . l-1 . min-1, and heart rate did not change. After ganglionic blockade (hexamethonium 40 mg/kg), norepinephrine increased mean arterial pressure by 76 +/- 3 mmHg, total peripheral resistance by 47 +/- 4 mmHg X l-1 X min-1, and heart rate did not change. Only after elimination of the buffering by heart rate by use of cholinergic receptor blockade (atropine 0.1 mg/kg) or ventricular pacing could buffering of the vasoconstrictor responses to alpha-adrenergic receptor agonists be demonstrated. Thus in conscious dogs the primary mechanism for buffering increases in arterial pressure induced by alpha-adrenergic receptor agonists is compensatory changes in heart rate and cardiac output with little buffering of total peripheral resistance.

Alpha2A adrenergic receptor‐mediated inhibition of mouse hippocampal CA3 network activity

2008 ◽  
Vol 22 (S2) ◽  
pp. 98-98
Author(s):  
Elizabeth Luger ◽  
Kylie Davis ◽  
Brianna Goldenstein ◽  
Brian Nelson ◽  
Ke Xu ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Network Activity ◽  
Hippocampal Ca3

β1 Adrenergic Receptor-Mediated Enhancement of Hippocampal CA3 Network Activity

2005 ◽  
Vol 314 (2) ◽  
pp. 552-560 ◽  
Author(s):  
Chris W. D. Jurgens ◽  
Katie E. Rau ◽  
Chris A. Knudson ◽  
Jacob D. King ◽  
Patrick A. Carr ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Network Activity ◽  
Hippocampal Ca3

scholarly journals Alpha-adrenergic receptor agonists in terms of modern views on glaucoma monitoring and treatment

2019 ◽  
pp. 87-91
Author(s):  
V.P. Erichev ◽  
◽  
S.Yu. Petrov ◽  
A.V. Volzhanin ◽  
D.M. Safonova ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Agonists ◽  
Alpha Adrenergic Receptor

scholarly journals Alpha‐2A adrenergic receptor activation inhibits rat hippocampal CA3 network activity

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Kylie Davis ◽  
Jessica Lichter ◽  
Brian Nelson ◽  
Brianna Goldenstein ◽  
Sarah Boese ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Network Activity ◽  
Hippocampal Ca3

DIAPHRAGMATIC FATIGUE RECOVERY IS ACCELERATED BY INSULIN AND ALPHA-ADRENERGIC RECEPTOR AGONISTS

1989 ◽  
Vol 71 (Supplement) ◽  
pp. A1125
Author(s):  
S. Glusman ◽  
A. Perez ◽  
A. Polk ◽  
E. Faure
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Agonists ◽  
Alpha Adrenergic Receptor ◽  
Diaphragmatic Fatigue ◽  
Fatigue Recovery
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