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

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.

1992 ◽  
Vol 208 (2) ◽  
pp. 333-339 ◽  
Author(s):  
Timothy PARR ◽  
Ronald G. BARDSLEY ◽  
R. Stewart GILMOUR ◽  
Peter J. BUTTERY

1978 ◽  
Vol 44 (2) ◽  
pp. 190-194 ◽  
Author(s):  
A. Koo ◽  
I. Y. Liang

The microcirculation of the spinotrapezius muscle in normal and cold-acclimated (4 degrees C) rats was observed by an in vivo microscopic technique. The responses of the arterioles and venules in the skeletal muscle microcirculation to topical application of norepinephrine (NE) were recorded by a photomicrographic method. Results show that the skeletal muscle microcirculation possesses both alpha- and beta-adrenergic vascular receptors. Stimulation of the alpha-receptor results in vasoconstriction, and of the beta-receptor, vasodilatation. These microvascular responses are antagonized by specific alpha- and beta-adrenergic blockers. Cold-acclimation (4 degrees C) for 3 wk decreases the responses of the skeletal muscle microvessels to NE stimulation. This diminished sensitivity is due to an attenuation of the alpha-adrenergic receptor mechanism.


1986 ◽  
Vol 250 (2) ◽  
pp. H221-H225 ◽  
Author(s):  
K. G. Proctor ◽  
S. L. Bealer

Transverse (3rd-order) arterioles (diam 12 +/- 2 micron, n = 6) in rat spinotrapezius muscle were observed with video microscopy during electrical stimulation of preoptic recess in periventricular region of hypothalamus (AV3V region) to test whether active skeletal muscle vasodilation was mediated by a beta-adrenergic mechanism. Bipolar wire electrodes were implanted in AV3V 3-7 days before an experiment. Continuous superfusion of propranolol (10(-5) M) caused steady-state reduction (3 +/- 1 microns) in arteriolar diameter and reduced steady-state vasodilation (26 +/- 2 vs. 11 +/- 2 microns) caused by a continuous superfusion of isoproterenol (10(-6) M). Six arterioles were observed with and without propranolol during four frequencies of AV3V stimulation (8-15 V, 0.2-0.5 ms pulse duration; 10, 15, 20, and 25 Hz; 1 min stimulus duration). Stimulation caused frequency-related reductions in arterial blood pressure (10-20 mmHg), which were sustained and not altered by propranolol. Transient peak diameters were observed after 30 +/- 7 s; the time was not related to stimulus frequency or affected by propranolol. Peak diameters averaged 14-17 microns during vehicle and 11-12 micron during propranolol (maximum diam 32 +/- 3). Peak vasodilations were significant but identical with vehicle or propranolol (avg 3 +/- 1 microns) and not related to stimulus frequency. Diameters stabilized at steady-state values above base line only during 15 and 20 Hz with vehicle and only during 20 Hz with propranolol. We conclude that AV3V stimulation causes transient vasodilation in spinotrapezius muscle that is probably not mediated by beta-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)


1982 ◽  
Vol 243 (4) ◽  
pp. E305-E309
Author(s):  
E. W. Chideckel ◽  
S. J. Rosovski ◽  
E. B. Belur

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.


1971 ◽  
Vol 68 (1_Suppla) ◽  
pp. S5-S38 ◽  
Author(s):  
Helmuth Vorherr

ABSTRACT In lactating rats and rabbits the mode of antagonism of sympathomimetics, angiotensin or pain toward oxytocin-induced milk-ejection was investigated. In rats intra-arterial (intrafemoral) doses of 0.01–0.02 μg or intravenous (iv) doses of 0.1–0.5 μg of either epinephrine, isoproterenol, norepinephrine, angiotensin or 10 μg of phenylephrine injected simultaneously with, or 30 seconds before an oxytocin dose (10 μU intrafemoral, 300 μU iv) greatly inhibited or suppressed the oxytocin response. A 15 second pain stimulus caused moderate inhibition. With alpha-receptor blockade pain, epinephrine, isoproterenol, norepinephrine, phenylephrine and angiotensin inhibition were, respectively, 70%, 75%, 100%, 40%, 0% and 100%. Under beta-receptor blockade the corresponding values were 14%, 40%, 0%, 70%, 100% and 100%; with simultaneous intrafemoral injections neither catecholamine was inhibitory toward oxytocin. In corresponding rabbit experiments approximately 10-fold higher iv drug dosages were applied and similar results were observed. In both species, combined alpha and beta-receptor blockade nearly eliminated the antagonistic actions of sympathomimetics toward oxytocin, whereas angiotensin inhibition persisted unchanged. The results indicate: 1) Mammary myoepithelial cells contain beta-adrenergic receptors but no alpha-receptors; 2) Inhibition of oxytocin-induced milk-ejection by isoproterenol and phenylephrine is meditated through stimulation of myoepithelial beta-receptors (myoepithelial relaxation) and vascular alpha-receptors (vasoconstriction), respectively; 3) Epinephrine and norepinephrine inhibition of milk-ejection is due to stimulation of vascular alpha-receptors and myoepithelial beta-receptors; 4) Angiotensin effects are unrelated to adrenergic receptor mechanisms; 5) Administration of both alpha and beta-adrenergic blockers is desirable for stabilizing the sensitivity of the oxytocin milk-ejection assay preparation against interference from endogenous or exogenous catecholamines; 6) Other than using adrenergic blockers, pharmacologic doses of oxytocin can correct nursing difficulties in animals and man with hyperfunction of the adrenal-sympathetic system.


FEBS Letters ◽  
1990 ◽  
Vol 259 (2) ◽  
pp. 269-272 ◽  
Author(s):  
F.Norman Briggs ◽  
K.Francis Lee ◽  
Joseph J. Feher ◽  
Andrew S. Wechsler ◽  
Kay Ohiendieck ◽  
...  

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