Circadian cycles in binding of 3H-alprenolol to β-adrenergic receptor sites in rat pineal

Nature ◽  
1975 ◽  
Vol 258 (5534) ◽  
pp. 435-436 ◽  
Author(s):  
J. A. ROMERO ◽  
M. ZATZ ◽  
J. W. KEBABIAN ◽  
J. AXELROD
1970 ◽  
Vol 23 (03) ◽  
pp. 417-422 ◽  
Author(s):  
D. G McKay ◽  
J.-G Latour ◽  
Mary H. Parrish

SummaryThe infusion of epinephrine in high doses produces disseminated intravascular coagulation by activation of Hageman factor. The effect is blocked by phenoxybenz-amine and is therefore due to stimulation of α-adrenergic receptor sites.


1982 ◽  
Vol 242 (3) ◽  
pp. R185-R188
Author(s):  
R. G. Carroll ◽  
D. F. Opdyke ◽  
N. E. Keller

In vivo infusion of MgCl2 blocks the dogfish pressor response to K+. This action of Mg2+ was contrasted to phentolamine in in vivo and in vitro experiments. Mg2+ blocks the spontaneous release of catecholamines from dogfish chromaffin tissue but does not alter the norepinephrine-induced contraction of the isolated dogfish artery. In vivo infusion of Mg2+ causes a significant decrease in resting catecholamine levels and diminishes the catecholamine release caused by K+ challenge. Both Mg2+ and phentolamine block the pressor action of K+, Mg2+ by preventing the K+-induced release of catecholamines and phentolamine by preventing the circulating catecholamines from interacting with alpha-adrenergic receptor sites.


1982 ◽  
Vol 90 (2) ◽  
pp. 233-236 ◽  
Author(s):  
Gary L. Schechter ◽  
David Arthur Brase ◽  
Jeffrey Powell

This report describes four patients who had early reversal of local anesthetic and vasoconstrictor effects during nasal surgery. They were all taking tricyclic antidepressants. The basic physiology of adrenergic receptor sites and the pharmacology of tricyclic antidepressants as they relate to catecholamine uptake are presented. An explanation of the adverse effect of the tricyclics is presented based on the concept of “epinephrine-reversal. “


1973 ◽  
Vol 29 (01) ◽  
pp. 011-026 ◽  
Author(s):  
Donald G McKay

SummaryThe generalized Shwartzman reaction is a definitive disease process which is the result of two minor episodes of acute inflammation of the circulating blood. The identifying feature of the reaction is thrombosis of the micro circulation, specifically of glomerular capillary thrombosis which persists long enough to cause bilateral renal cortical necrosis. The reaction is the result of an interplay between leukocytes, platelets, complement, the contact system, the extrinsic prothrombin activator system, adrenal glucocorticoids, adrenal catecholamines, alpha - adrenergic receptor sites and the fibrinolytic enzyme system. The reaction occurs only when these systems are affected within narrow quantitative limits. It is a model of the effects of bacterial endotoxin on the blood-vascular system and has important implications for acute inflammatory episodes of the circulating blood induced by other inflammatory agents such as antigen-antibody complex and particulate matter.


1970 ◽  
Vol 116 (533) ◽  
pp. 435-436 ◽  
Author(s):  
Tito Campanini ◽  
Alberto Catalano ◽  
Carlo De Risio ◽  
Giacomo Mardighian

The catecholamine hypothesis of affective disorders proposes that 'some-if not all-depressions are associated with an absolute or relative decrease in catecholamines, particularly norepinephrine, available at central adrenergic receptor sites. Elation, conversely, may be associated with an excess of such amines' (Schildkraut, 1965).


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