Catecholamine-thyroid hormone interaction on myocardial ornithine decarboxylase

1982 ◽  
Vol 243 (4) ◽  
pp. E305-E309
Author(s):  
E. W. Chideckel ◽  
S. J. Rosovski ◽  
E. B. Belur
Keyword(s):  
Thyroid Hormone ◽  
Ornithine Decarboxylase ◽  
Inhibitory Effect ◽  
Alpha Activity ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Hyperthyroid Heart ◽  
Increased Activity ◽  
Fasted Rats ◽  
Stimulation Of

Myocardial phosphorylase alpha activity responds to stimulation by catecholamines and thyroid hormone. In hyperthyroidism this enzyme is supersensitive to beta-adrenergic stimulation and blockade, indicating that its increased activity is an indirect effect of thyroid hormone. Myocardial ornithine decarboxylase (ODC) activity also responds to catecholamine and thyroid hormone stimulation. In the present studies, we sought to determine whether ODC shares the responses of phosphorylase alpha in hyperthyroidism. As opposed to euthyroid rats, isoproterenol acutely inhibited myocardial OCD activity in hyperthyroid rats. Timolol (60 mg/kg) injected immediately before the isoproterenol blocked this paradoxical inhibitory effect, defining it as beta-adrenergic. When timolol (100 mg/kg), distributed over a 24-h period, was administered during the 3 days of triiodothyronine (T3) administration, it blocked the T3 stimulation of myocardial OCD activity by 35%. However, timolol affected weight gain of the hyperthyroid rats. When fasted rats were used, timolol was without effect on T3-induced myocardial ODC stimulation. Timolol was also without effect on T3-induced stimulation of hepatic ODC or on T3-induced cardiomegaly. Timolol did decrease the T3-induced tachycardia. In summary, in the hyperthyroid heart, 1) isoproterenol paradoxically inhibits myocardial ODC activity and 2) timolol, when food intake is not a variable, is without effect. We conclude that the effect of thyroid hormone on myocardial ODC is not mediated by change in catecholamine sensitivity. Thus the behavior of phosphorylase alpha does not represent a general enzymatic phenomenon.

ANTAGONISM BETWEEN INSULIN AND SELECTIVE ADRENERGIC AGONISTS ON THE GLYCOGEN SYNTHETASE AND PHOSPHORYLASE SYSTEMS OF THE ISOLATED RAT DIAPHRAGM

1975 ◽  
Vol 78 (2) ◽  
pp. 392-400
Author(s):  
Arne T. Hostmark ◽  
Ole Grønnerød ◽  
Robert S. Horn
Keyword(s):  
Glycogen Metabolism ◽  
Rat Diaphragm ◽  
Adrenergic Agonists ◽  
Adrenergic Stimulation ◽  
Insulin Effect ◽  
Glycogen Synthetase ◽  
Adrenergic Antagonists ◽  
Fasted Rats ◽  
Isolated Rat ◽  
Stimulation Of

ABSTRACT The antagonism between insulin and selective adrenergic stimulation on the converting systems for glycogen synthetase and phosphorylase has been investigated in the isolated rat diaphragm. Insulin significantly inhibited stimulation by terbutaline and noradrenaline of phosphorylase b to a conversion as well as stimulation of glycogen synthetase I to D conversion by these agents. The inhibition by insulin was stronger on the synthetase system than on the phosphorylase system. The insulin effect was not dependent upon the presence of glucose. In diaphragms from 24 h fasted rats the response of the phosphorylase system to both agonists decreased. Inhibition by insulin of terbutaline stimulated phosphorylase conversion was maintained upon fasting while no effect of insulin against stimulation by noradrenaline could be obtained in diaphragms from fasted rats. The effects of fasting and insulin were not influenced by beta adrenergic antagonists (practolol and butoxamine). The results indicate a difference in sensitivity of the synthetase and phosphorylase systems to insulin and suggest that noradrenaline and terbutaline influence glycogen metabolism by differing mechanisms.

Effects of epinephrine on insulin-stimulated glucose uptake and GLUT-4 phosphorylation in muscle

1997 ◽  
Vol 273 (3) ◽  
pp. C1082-C1087 ◽  
Author(s):  
A. D. Lee ◽  
P. A. Hansen ◽  
J. Schluter ◽  
E. A. Gulve ◽  
J. Gao ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Glucose Transport ◽  
Glucose Transporter ◽  
Inhibitory Effect ◽  
Phosphate Concentration ◽  
Intrinsic Activity ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Glut 4

beta-Adrenergic stimulation has been reported to inhibit insulin-stimulated glucose transport in adipocytes. This effect has been attributed to a decrease in the intrinsic activity of the GLUT-4 isoform of the glucose transporter that is mediated by phosphorylation of GLUT-4. Early studies showed no inhibition of insulin-stimulated glucose transport by epinephrine in skeletal muscle. The purpose of this study was to determine the effect of epinephrine on GLUT-4 phosphorylation, and reevaluate the effect of beta-adrenergic stimulation on insulin-activated glucose transport, in skeletal muscle. We found that 1 microM epinephrine, which raised adenosine 3',5'-cyclic monophosphate approximately ninefold, resulted in GLUT-4 phosphorylation in rat skeletal muscle but had no inhibitory effect on insulin-stimulated 3-O-methyl-D-glucose (3-MG) transport. In contrast to 3-MG transport, the uptakes of 2-deoxyglucose and glucose were markedly inhibited by epinephrine treatment. This inhibitory effect was presumably mediated by stimulation of glycogenolysis, which resulted in an increase in glucose 6-phosphate concentration to levels known to severely inhibit hexokinase. We conclude that 1) beta-adrenergic stimulation decreases glucose uptake by raising glucose 6-phosphate concentration, thus inhibiting hexokinase, but does not inhibit insulin-stimulated glucose transport and 2) phosphorylation of GLUT-4 has no effect on glucose transport in skeletal muscle.

beta-Adrenergic stimulation of respiratory ciliary activity

1980 ◽  
Vol 48 (5) ◽  
pp. 868-871 ◽  
Author(s):  
P. Verdugo ◽  
N. T. Johnson ◽  
P. Y. Tam
Keyword(s):  
Respiratory Epithelium ◽  
Ciliary Activity ◽  
Ciliated Cells ◽  
Adrenergic Stimulation ◽  
Laser Scattering ◽  
Beta Adrenergic ◽  
Ciliary Beating ◽  
Stimulation Of

We investigated the effect of isoproterenol on ciliary activity using a mucus-free preparation of cultured ciliated cells of the rabbit trachea. The frequency of ciliary beating was monitored by dynamic laser-scattering spectroscopy. The results demonstrated that isoproterenol directly stimulates the activity of ciliated cells of the respiratory epithelium and that this effect is beta-adrenergic specific inasmuch as the observed stimulation can be blocked by propranolol.

Effect of norepinephrine on consumption of oxygen in perfused skeletal muscle from cold-exposed rats

1988 ◽  
Vol 254 (4) ◽  
pp. E482-E489 ◽  
Author(s):  
M. Shiota ◽  
S. Masumi
Keyword(s):  
Skeletal Muscle ◽  
Beta Adrenergic ◽  
Control Muscle ◽  
Exposure To Cold ◽  
Net Uptake ◽  
Increased Activity ◽  
Net Release ◽  
Stimulation Of

The effect of norepinephrine on the consumption of O2 was studied in the skeletal muscle in the perfused hindlimbs of rats that had been kept at 4 degrees C for 5-25 days. 1) Basal rates of consumption of O2 and release of lactate were not affected by exposure to cold. 2) The stimulation of consumption of O2 by norepinephrine increased in the perfused hindlimbs of rats exposed to cold for 10-25 days, with a maximum stimulation at 20 days. The response to norepinephrine decreased markedly in hindlimbs perfused with propranolol or phentolamine. Phenylephrine, in the presence of 0.5 nM isoproterenol, stimulated the consumption of O2 at concentrations as low as 0.5 microM, with a maximum at 5 microM, in hindlimbs from the group exposed to cold for 20 days. 3) Ouabain inhibited the stimulation of consumption of O2 by norepinephrine. Norepinephrine caused a net release of K+ in control muscle but a net uptake of K+ by muscle from the group exposed to cold for 20 days. The results suggest that the calorigenic responsiveness to norepinephrine increases in skeletal muscle during acclimation of the rat to the cold, both alpha- and beta-adrenergic actions are involved in the calorigenic effects of norepinephrine, and the increased activity of the Na+-K+ ATPase under the influence of norepinephrine may be involved in the calorigenic action of norepinephrine on the skeletal muscle of cold-acclimated rats.

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