Beta-adrenergic mechanisms in the nasal mucosa vascular bed

1995 ◽  
Vol 252 (5) ◽  
Author(s):  
J.S. Lacroix ◽  
A.M. Kurt ◽  
S. Auberson ◽  
C. Bretton
Keyword(s):  
Nasal Mucosa ◽  
Beta Adrenergic ◽  
Adrenergic Mechanisms ◽  
Vascular Bed

Adrenergic mechanisms in the cerebral vascular bed

1973 ◽  
Vol 29 (6) ◽  
pp. 675-676 ◽  
Author(s):  
A. Juhász-Nagy ◽  
G. Bock
Keyword(s):  
Adrenergic Mechanisms ◽  
Vascular Bed ◽  
Cerebral Vascular

Beta-Adrenergic Mechanisms in Action Tremor

1975 ◽  
Vol 293 (19) ◽  
pp. 950-953 ◽  
Author(s):  
Robert R. Young ◽  
John H. Growdon ◽  
Bhagwan T. Shahani
Keyword(s):  
Action Tremor ◽  
Beta Adrenergic ◽  
Adrenergic Mechanisms

Alpha- and beta-adrenergic mechanisms in the control of vascular capacitance by the carotid sinus baroreflex system

1994 ◽  
Vol 267 (1) ◽  
pp. H201-H210 ◽  
Author(s):  
K. Shigemi ◽  
M. J. Brunner ◽  
A. A. Shoukas
Keyword(s):  
Adrenergic Receptor ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Systemic Circulation ◽  
Adrenergic System ◽  
Beta Adrenergic ◽  
Vascular Volume ◽  
Adrenergic Mechanisms ◽  
Vascular Capacitance ◽  
Carotid Sinus Baroreflex

We examined the active and passive contributions of the alpha- and beta-adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an alpha- (phentolamine) or a beta- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 +/- 9.0 ml/kg without any antagonist) was reduced by 72% with phentolamine, by 35% with propranolol, and by 73% with both antagonists. Our results suggest that the alpha-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the beta-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.

Role of Beta-Adrenergic Mechanisms in Exercise Training-Induced Metabolic Changes in Respiratory and Locomotor Muscle

1995 ◽  
Vol 16 (01) ◽  
pp. 13-18 ◽  
Author(s):  
S. Powers ◽  
M. Wade ◽  
D. Criswell ◽  
R. Herb ◽  
S. Dodd ◽  
...  
Keyword(s):  
Exercise Training ◽  
Metabolic Changes ◽  
Beta Adrenergic ◽  
Adrenergic Mechanisms

Eicosonoid metabolism and beta-adrenergic mechanisms in coronary arterial smooth muscle: potential compartmentation of cAMP

1986 ◽  
Vol 250 (3) ◽  
pp. C406-C412 ◽  
Author(s):  
G. Rubanyi ◽  
P. Galvas ◽  
J. DiSalvo ◽  
R. J. Paul
Keyword(s):  
Arachidonic Acid ◽  
Glycogen Phosphorylase ◽  
Isometric Force ◽  
Phosphorylase Activity ◽  
Straightforward Manner ◽  
Beta Adrenergic ◽  
Camp Content ◽  
Adrenergic Mechanisms ◽  
Proposed Model ◽  
Muscle Potential

Beta-Adrenergic relaxation in bovine coronary arteries is enhanced by inhibition of eicosonoid metabolism and inhibited by its stimulation. We investigated the interaction between eicosonoid metabolism and beta-adrenergic mechanisms by studying the effect of perturbations of eicosonoid metabolism on vascular adenosine 3',5'-monophosphate (cAMP) content and the cAMP-dependent relaxation of isometric force and activation of glycogen phosphorylase. KCl (35 mM) elicited a contraction, activated phosphorylase, and slightly decreased cAMP content. Isoproterenol (10(-7) M) relaxed the KCl contraction, further increased phosphorylase activity, and increased cAMP. Neither indomethacin (5 X 10(-6) M) nor arachidonic acid (3 X 10(-5) M) affected the KCl contraction, but arachidonic acid increased both cAMP and phosphorylase activity and indomethacin decreased cAMP. Indomethacin potentiated the relaxation induced by isoproterenol but inhibited the activation of phosphorylase and had no effect on the isoproterenol-induced increase in cAMP. Arachidonic acid, on the other hand, inhibited the isoproterenol-induced relaxation but potentiated both the increases of phosphorylase activity and cAMP. Thus neither relaxation nor phosphorylase activity was related in a straightforward manner to the total cAMP content. A direct relation between cAMP, relaxation, and phosphorylase can be reconciled with the antiparallel effects of alterations of eicosonoid metabolism observed in this study by a proposed model in which the effects of cAMP are assumed to be functionally compartmentalized.

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