Acute effect of epinephrine on muscle proteolysis in perfused rat hindquarters

1996 ◽  
Vol 270 (6) ◽  
pp. E961-E967 ◽  
Author(s):  
M. Kadowaki ◽  
T. Kamata ◽  
T. Noguchi
Keyword(s):  
Perfusion Pressure ◽  
Initial Rate ◽  
Sharp Decrease ◽  
Acute Effect ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Intracellular Pool ◽  
Beta Adrenoceptor ◽  
Adrenergic Activity ◽  
Rate Infusion

An acute and direct effect of epinephrine (Epi) on muscle proteolysis was investigated using a single-pass mode of rat hindquarter perfusion. The rate of tyrosine (Tyr) release at > 30 min with cycloheximide was regarded as the muscle proteolytic rate. Infusion of Epi (500 nM) to the hindquarters of fed rats led to a sharp decrease in the Tyr release to 50% within 5 min, accompanied by an increase in perfusion pressure and edema around the perfused tissues. To clarify the mechanism, alpha- and beta-antagonists were used together with Epi. A mixture of 10 microM prazosin and 10 microM yohimbine (alpha-adrenergic blockade) before or after Epi infusion completely prevented the edema development and resulted in a new steady state to 80% of the initial rate. On the contrary, 100 microM propranolol (a beta-antagonist) with Epi did not abolish the edema and caused fluctuation in Tyr release. Whether the above results are affected by changes in Tyr transport at the plasma membrane was tested by measuring Tyr efflux from the perfused muscle. Only a beta-adrenergic blockade significantly reduced the rate constant of Tyr efflux from the intracellular pool by 13%. These results suggested that the suppression of Tyr release by alpha-adrenergic activity was mainly due to the effect on Tyr efflux, whereas that by beta-adrenergic activity was not at the Tyr transport level but at the proteolysis level, demonstrating that Epi directly inhibits proteolysis of skeletal muscle via the beta-adrenoceptor.

Failure of chronic beta-adrenergic blockade to inhibit overfeeding-induced thermogenesis in humans

1989 ◽  
Vol 256 (3) ◽  
pp. R653-R658 ◽  
Author(s):  
S. L. Welle ◽  
K. S. Nair ◽  
R. G. Campbell
Keyword(s):  
Weight Maintenance ◽  
Resting Metabolic Rate ◽  
Control Group ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Initial Reduction ◽  
Adrenergic Antagonist ◽  
Adrenergic Activity ◽  
Propranolol Treatment ◽  
Male Subjects

The effect of the beta-adrenergic antagonist propranolol on the increase in resting metabolic rate (RMR) induced by overfeeding was examined to determine whether increased beta-adrenergic activity contributes to this response. Six male subjects who were overfed with carbohydrate (1,600 excess kcal/day) for 10 days without drug treatment (control group) had increases (compared with values after 10 days of weight maintenance) in RMR after 6 days [0.24 +/- 0.06 kcal/min (22%)] and 10 days of overfeeding [0.17 +/- 0.03 kcal/min (15%)]. Eight male subjects were given a weight-maintenance diet for 10 days with oral propranolol treatment (40-60 mg every 6 h) over the last 7 days of this period. Five of these subjects were then overfed for 10 days, and three remained on the weight-maintenance diet; propranolol treatment continued until the end of the study. Propranolol significantly reduced RMR (mean 9%) before the onset of overfeeding but did not prevent increases in RMR after 6 days [0.18 +/- 0.05 kcal/min (16%)] and 10 days of overfeeding [0.17 +/- 0.03 kcal/min (15%)]. In the subjects who remained on the weight-maintenance diet throughout the study, there was no reversal of propranolol's initial reduction of RMR that would have falsely elevated the overfeeding effect. These data provide further evidence that the increase in RMR induced by overfeeding in humans is not mediated by increased beta-adrenergic activity.

Beta-adrenergic blockade and training in human subjects: effects on muscle metabolic capacity

1984 ◽  
Vol 247 (3) ◽  
pp. E305-E311 ◽  
Author(s):  
J. Svedenhag ◽  
J. Henriksson ◽  
A. Juhlin-Dannfelt
Keyword(s):  
Placebo Group ◽  
Citrate Synthase ◽  
Human Subjects ◽  
Capillary Density ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Mitochondrial Enzymes ◽  
Beta Adrenergic ◽  
Beta Adrenoceptor ◽  
Cyt C

Sixteen male subjects (20–31 yr) trained for 8 wk on cycle ergometers. Eight of the subjects were treated during the training period with the beta-adrenoceptor blocker propranolol (160 mg/day). During all pre-and posttraining tests, subjects were uninfluenced by the medication. Training-induced increases in VO2max and decreases in blood lactate and norepinephrine concentrations at submaximal exercise were not different between the beta-blockade and the placebo groups. The activities of the mitochondrial enzymes citrate synthase (CS), succinate dehydrogenase (SDH), cytochrome c oxidase (Cyt-c-ox), and 3-hydroxyacyl-CoA dehydrogenase (HAD) in the quadriceps femoris muscle increased significantly (P less than 0.01) with training (beta-blockade group, +47, +33, +38, and 22%; placebo group, +75, 70, +87, and +63%, respectively). Cyt-c-ox and HAD increased significantly more in the placebo group than in the beta-blockade group, while a tendency to an increase was noted for SDH. Muscle capillary density increased similarly (+17–19%) with training in the two groups (P less than 0.01). In conclusion, subjects training under the influence of a therapeutic level of beta-adrenergic blockade show marked increases in both the respiratory capacity and the capillary supply of the engaged skeletal muscles. However, the increase in muscle mitochondrial enzymes may be less apparent than in the normal state.

Physiological antagonism caused by adrenergic stimulation of canine tracheal muscle

1986 ◽  
Vol 60 (1) ◽  
pp. 216-224 ◽  
Author(s):  
A. R. Leff ◽  
J. Tallet ◽  
N. M. Munoz ◽  
N. Shoulberg
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Contraction ◽  
Tracheal Smooth Muscle ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Beta Adrenoceptor ◽  
Response Characteristics ◽  
Stimulation Of

We studied the simultaneous alpha- and beta-adrenergic response characteristics of canine tracheal smooth muscle in 398 strips from 67 dogs in vitro. Experiments were performed to determine the effects of beta-adrenergic blockade on the expression of the alpha-adrenoceptor contractile responses elicited by norepinephrine (NE), phenylephrine (PE), and clonidine (CLO). Maximal active tension caused by NE increased from 39.1 +/- 27.0 to 241 +/- 75.0 g/cm2 as the concentration of propranolol (PROP) was increased from 10(-6) to 10(-4) M. Augmentation of tracheal smooth muscle contraction caused by PE and CLO was also observed with progressive beta-adrenoceptor blockade; contraction to NE, PE, and CLO was blocked selectively with 3 X 10(-5) M phentolamine (PA) and phenoxybenzamine (PBZ). The beta-adrenergic relaxing properties of the same three agonists were also studied. After alpha-adrenergic blockade with PA or PBZ, all three agonists caused relaxation (NE greater than CLO greater than PE) of methacholine-induced contraction of tracheal smooth muscle that was reversed selectively with PROP. We demonstrate that NE, PE, and CLO cause simultaneous stimulation of both the alpha- and beta-adrenergic receptors in tracheal smooth muscle; the net response elicited is the result of adrenergic physiological antagonism and depends on the relative degree of alpha- and/or beta-adrenoceptor blockade.

The Inhibition of Renin Secretion by Alpha-Adrenergic Stimulation in the Isolated Rat Kidney

1974 ◽  
Vol 47 (5) ◽  
pp. 471-479 ◽  
Author(s):  
R. Vandongen ◽  
W. S. Peart
Keyword(s):  
Adrenergic Receptors ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Blocking Agent ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Renal Perfusion Pressure ◽  
Adrenergic Activity

1. The respective role of alpha-adrenergic and beta-adrenergic receptors in mediating the effect of catecholamines on renin secretion was examined in the isolated perfused rat kidney. 2. Noradrenaline, which has combined alpha- and beta-adrenergic activity, stimulated renin secretion only in the presence of the alpha-receptor blocking agent phenoxybenzamine. This stimulatory effect was largely prevented by the addition of the beta-blocking agent, propranolol. The vasoconstrictor action of noradrenaline, and thus the rise in mean renal perfusion pressure, was abolished by phenoxybenzamine. Our previous finding that noradrenaline alone stimulated renin release was inconclusive (Vandongen, Peart & Boyd, 1973). 3. Noradrenaline stimulated renin secretion when calcium was excluded from the perfusion fluid, to which disodium EDTA (25 mmol/l) was added. The vasoconstrictor action of noradrenaline was considerably attenuated under these conditions. 4. Methoxamine, which has only alpha-adrenergic activity, did not increase renin secretion when infused alone or with phenoxybenzamine. The increase in renin secretion after beta-adrenergic stimulation with isoproterenol was significantly suppressed by methoxamine, although this was associated with an increase in mean renal perfusion pressure. 5. These findings indicate the importance of intrarenal beta-adrenergic receptors in the stimulation of renin secretion and suggest that an opposite inhibitory effect on renin secretion follows alpha-adrenergic activity. 6. Although the results do not exclude a direct effect of vascular tone and renal perfusion pressure, it is suggested that the stimulation and inhibition of renin secretion is related to smooth muscle activity by the involvement of a calcium-dependent process similar to that involved in contraction and relaxation. This would accord with the common derivation of the renin-producing and vascular smooth muscle cells

Inhibitory effect of plasma free fatty acids on glucose production in the conscious dog

1984 ◽  
Vol 246 (2) ◽  
pp. E181-E186
Author(s):  
R. R. Wolfe ◽  
J. H. Shaw
Keyword(s):  
Glucose Production ◽  
Plasma Free Fatty Acid ◽  
Inhibitory Effect ◽  
Hormonal Control ◽  
Constant Infusion ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Adrenergic Activity ◽  
Plasma Ffa ◽  
Production Response

We have previously reported that, in conscious, unrestrained dogs in which insulin and glucagon levels were clamped pharmacologically, combined alpha- and beta-adrenergic blockade resulted simultaneously in a fall in plasma free fatty acid (FFA) levels and an increase in glucose production. In this study we have tested the hypothesis that the increase in glucose production observed in the previous study was due to the fall in plasma FFA concentration. Glucose production was measured by means of the primed-constant infusion of [6-3H]- and/or [U-14C]glucose, and insulin and glucagon were clamped at constant levels by means of the infusion of somatostatin, insulin, and glucagon. When no attempt was made to control the FFA levels, combined alpha- and beta-adrenergic blockade significantly decreased plasma FFA levels, and this was associated with a significant increase in the rate of glucose production. However, the glucose production response to adrenergic blockade was entirely prevented by the clamping of FFA levels at a high, constant value by the infusion of a 10% lipid emulsion (Liposyn) and heparin. We conclude that basal adrenergic activity is important in the mobilization of fat but does not directly influence glucose production. Further, there is an inhibitory effect of FFA on glucose production that is unmasked during hormonal control and alpha- and beta-adrenergic blockade.

Enhanced beta-adrenergic-receptor responsiveness in hypoxic neonatal pulmonary circulation

1981 ◽  
Vol 240 (5) ◽  
pp. H697-H703 ◽  
Author(s):  
J. E. Lock ◽  
P. M. Olley ◽  
F. Coceani
Keyword(s):  
Pulmonary Circulation ◽  
Beta Blockade ◽  
Base Line ◽  
Pulmonary Resistance ◽  
Beta Adrenergic ◽  
Beta Receptor ◽  
Adrenergic Activity ◽  
Alpha Blockade ◽  
Alveolar Hypoxia ◽  
Constrictor Response

The influence of alveolar hypoxia on pulmonary vascular adrenergic receptors was studied in conscious newborn lambs. In control animals, pulmonary vessels were directly constricted by epinephrine and norepinephrine, but were unaffected by isoproterenol. Pulmonary resistance (PVR) was also unaffected by propranolol, thus implying minimal beta-receptor activity under normoxic conditions. Hypoxia raised PVR but also modified the pulmonary vascular responses to catecholamines: isoproterenol became a dilator, whereas the constrictor effects of epinephrine and norepinephrine were abolished. Although beta-blockade did not alter base-line PVR, propranolol increased the constrictor response to hypoxia, implying that hypoxia increases beta-adrenergic activity or reactivity in the pulmonary circulation. Consistent with this hypothesis are the following: 1) in alpha-blocked lambs, epinephrine was without local effects during normoxia, but caused vasodilation during hypoxia; 2) the absent constrictor response to epinephrine during hypoxia is fully restored by propranolol; and 3) although alpha-blockade blunts the hypoxic constrictor response, the full response is restored when beta-blockade is added. These results indicate that the hypoxic constrictor response is partially opposed by increased beta-mediated vasodilation. These enhanced beta-receptor effects are due, at least in part, to increased beta-receptor reactivity of unknown mechanism.

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