Influnce of the beta-adrenergic agonist clenbuterol on plasma catecholamines and lymphocyte beta-receptors

1986 ◽  
Vol 1 (3) ◽  
pp. 234-236
Author(s):  
B. Bondy ◽  
M. Ackenheil ◽  
G. Laakmann ◽  
H.T. Munz
Keyword(s):  
Specific Binding ◽  
Plasma Catecholamines ◽  
Adrenergic System ◽  
Plasma Norepinephrine ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Receptors ◽  
Β Receptor ◽  
Beta Adrenergic Agonist ◽  
The Brain

SummaryThe influence of subchronic application of the β-adrenergic agonist clenbuterol on plasma norepinephrine (NE), epinephrine (E) and β-receptors on lymphocytes was investigated in 8 male, healthy volunteers. Treatment with clenbuterol (0.04 mg/day) for 6 days induced significant reduction of β-receptor specific binding in 7 of the 8 subjects with a mean decrease of 40% (p < 0.01) with no changes in affinity. Concomitantly an increase in the plasma NE concentration was observed (mean 50%, p < 0.01), but no significant overall alteration of E concentration. Our results suggest that β-adrenergic agonists exercise a similar effect on the peripheral adrenergic system and on the adrenergic system in the brain.

Effect of adrenergic agonists on big and small renin

1980 ◽  
Vol 238 (5) ◽  
pp. E416-E420
Author(s):  
H. Iwao ◽  
C. S. Lin ◽  
A. M. Michelakis
Keyword(s):  
Submaxillary Gland ◽  
Plasma Renin ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Molecular Weights ◽  
Submaxillary Glands ◽  
Beta Adrenergic Agonists ◽  
Beta Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

The effect of alpha- and beta-adrenergic agonists on renal and submaxillary renin of different molecular weights was studied using male albino mice as experimental animals. Phenylephrine or isoproterenol was administered intravenously after removal of the submaxillary glands and/or kidneys. Renin was isolated from plasma by column chromatography and then measured by a direct radioimmunoassay. Phenylephrine increased both 68,500-dalton renin (big renin) and 38,000-dalton renin (small renin) in the plasma of nephrectomized mice. Isoproterenol increased big and small renin in the plasma of mice whose submaxillary glands were removed. In both cases, the increase of small renin was significantly greater than that of big renin. The results suggest that the alpha-adrenergic agonist phenylephrine affects the submaxillary gland, leading to the increase of both big and small plasma renin. In contrast, the beta-adrenergic agonist isoproterenol affects the kidney, leading to the increase of both big and small plasma renin.

Angiotensin II receptors in SFO but not in OVLT mediate isoproterenol-induced thirst

1994 ◽  
Vol 267 (1) ◽  
pp. R7-R15 ◽  
Author(s):  
D. A. Fitts
Keyword(s):  
Angiotensin Ii ◽  
Circumventricular Organs ◽  
Ang Ii ◽  
Circumventricular Organ ◽  
Adrenergic Agonist ◽  
Receptor Sites ◽  
Organum Vasculosum Laminae Terminalis ◽  
Reduced Drinking ◽  
Beta Adrenergic Agonist ◽  
The Brain

Thirst elicited by the beta-adrenergic agonist isoproterenol in rats depends in part on the secretion of renin, the consequent synthesis of angiotensin II (ANG II), and the binding of circulating ANG II to dipsogenic receptors in the brain. These receptors probably reside in either of two forebrain circumventricular organs, the subfornical organ (SFO) or organum vasculosum laminae terminalis (OVLT). Experiments determined that lesions of the SFO, but not of the OVLT, reduced drinking induced by isoproterenol treatment. Competitive ANG II-receptor antagonism with sarthran reduced isoproterenol-induced drinking when the blocker was infused into the SFO but not when it was infused into the OVLT or into the lateral ventricles at a 25-fold greater dose. The findings confirm the widely held belief that renin-dependent thirst elicited by isoproterenol relies on ANG II binding to receptor sites at a circumventricular organ in the brain. The results demonstrate that this site is the SFO and not the OVLT.

The effect of feeding the beta-adrenergic agonist ractopamine on the behaviour of market-weight pigs

1992 ◽  
Vol 72 (1) ◽  
pp. 15-21 ◽  
Author(s):  
A. L. Schaefer ◽  
S. D. M. Jones ◽  
A. K. W. Tong ◽  
A. M. B. dePassille ◽  
J. Rushen ◽  
...  
Keyword(s):  
Aggressive Behaviour ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Treatment Groups ◽  
Beta Adrenergic Agonists ◽  
Key Words Pig ◽  
Ad Libitum ◽  
Beta Adrenergic Agonist ◽  
Effect Of Feeding

A total of 86 ad libitum fed Lacombe bred barrows and gilts weighing on average 90 kg were used to determine the effect of feeding ractopamine on animal behaviour. Four treatment groups consisted of a control (N = 22) and three levels of ractopamine (10 ppm (N = 15), 15 ppm (N = 24) and 20 ppm (N = 25) in the diet). The pigs received the ractopamine treatments for 5–6 wk prior to behavioural observations. There was little effect of ractopamine on behaviour. The ractopamine-fed pigs were observed to lie down in a group more frequently (P = 0.06) and to walk around their pen less frequently (P = 0.01). No abnormal, stereotyped, agonistic or aggressive behaviour was induced by the ractopamine. The data from the present study suggest that ractopamine, added to the diet of market-weight pigs at levels reported, does not cause marked changes in behaviour. Key words: Pig behaviour, beta-adrenergic agonists, ractopamine

Norepinephrine increases beta-receptors and adenylate cyclase in canine myocardium

1984 ◽  
Vol 246 (1) ◽  
pp. H31-H36 ◽  
Author(s):  
W. J. Raum ◽  
M. M. Laks ◽  
D. Garner ◽  
M. H. Ikuhara ◽  
R. S. Swerdloff
Keyword(s):  
Adenylate Cyclase ◽  
Myocardial Hypertrophy ◽  
Left Ventricular ◽  
Heart Weight ◽  
Adrenergic System ◽  
Plasma Norepinephrine ◽  
Beta Receptor ◽  
Norepinephrine Content ◽  
Beta Receptors ◽  
Canine Myocardium

Norepinephrine, a known inducer of myocardial hypertrophy, was found to have marked effects on the myocardial adrenergic system, which occurred prior to the development of a significant increase in heart weight. The chronic subhypertensive infusion (1.4 microgram/min) in free-roaming dogs produced a threefold increase in plasma norepinephrine (determined by radioimmunoassay). After 3 mo of infusion, right and left ventricular norepinephrine content (ng/mg protein) decreased significantly by twofold (right, 2.50 +/- 0.24; left, 2.08 +/- 0.36) compared with controls (right, 4.76 +/- 1.48; left, 4.65 +/- 1.49), and beta-receptor density (125I-pindolol) increased (right, 0.122 +/- 0.029; left, 0.153 +/- 0.021) over the controls (right, 0.082 +/- 0.015; left, 0.069 +/- 0.008 pmol/mg protein). Accompanying the beta-receptor changes, isoproterenol-stimulated adenylate cyclase activity also increased significantly [right, 29.2 +/- 2.1; left, 29.5 +/- 1.0 vs. controls, right, 13.8 +/- 1.1; left, 20.2 +/- 2.2 pmol adenosine 3',5'-cyclic monophosphate (cAMP) generated X min-1 X mg protein-1]. Because the above changes occurred in the absence of cardiac hypertrophy, it suggests that alterations in the myocardial adrenergic system are dependent on the stimulus (in this case norepinephrine) invoking the change and not the degree of hypertrophy. It also suggests that changes in the adrenergic system may not directly reflect the mechanism involved in the development of hypertrophy.

scholarly journals The activation of Na+-dependent efflux of Ca2+ from liver mitochondria by glucagon and β-adrenergic agonists

1983 ◽  
Vol 210 (2) ◽  
pp. 463-472 ◽  
Author(s):  
T P Goldstone ◽  
R J Duddridge ◽  
M Crompton
Keyword(s):  
Cyclic Amp ◽  
Liver Mitochondria ◽  
Ionophore A23187 ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Perfusion Medium ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonist

The Na+-induced efflux of Ca2+ from liver mitochondria was activated by tissue pretreatment with 1 microM-adrenaline, 1 microM-isoprenaline, 10 nM-glucagon and 100 microM-cyclic AMP when 10 mM-lactate plus 1 mM-pyruvate were present in the perfusion medium. Infusion of the alpha 1-adrenergic agonist, phenylephrine (10 microM), was ineffective. The activation induced by the beta-adrenergic agonist, isoprenaline, was maximal after infusion of agonist for 2 min. The isoprenaline-induced activation was very marked (120-220%), with about 7 nmol of intramitochondrial Ca2+/mg of protein, but was not evident with greater than 15 nmol of Ca2+/mg. Ca2+ efflux in the absence of Na+ and in the presence of the Ca2+ ionophore A23187 was not affected by isoprenaline pretreatment over the range 6-23 nmol of internal Ca2+/mg. With 10 mM-lactate plus 1 mM-pyruvate in the perfusion medium, glucagon and isoprenaline infusion increased tissue cyclic AMP content about 8-fold and 3-fold respectively. With 10 mM-pyruvate alone, neither glucagon nor isoprenaline caused a significant increase in cyclic AMP. Omission of lactate also abolished the ability of glucagon, but not of isoprenaline, to activate the Na+-induced efflux of Ca2+. The data indicate that cyclic AMP may mediate the activation caused by glucagon, but provide no evidence that cyclic AMP is an obligatory link in the beta-adrenergic-induced activation.

Sodium-independent modulation of Na(+)-K(+)-ATPase activity by beta-adrenergic agonist in alveolar type II cells

1995 ◽  
Vol 268 (6) ◽  
pp. L983-L990 ◽  
Author(s):  
S. Suzuki ◽  
D. Zuege ◽  
Y. Berthiaume
Keyword(s):  
Atpase Activity ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Alveolar Type Ii Cells ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonists ◽  
Beta Adrenergic Agonist

Although beta-adrenergic agonists are known to stimulate sodium transport in alveolar epithelial cells, the exact cellular mechanism involved in this process is unknown. We determined whether terbutaline, a beta-adrenergic agonist, modulated Na(+)-K(+)-ATPase in cultured rat alveolar type II cells by measuring the enzyme's activity via an adapted radiometric method. The assay conditions were optimized by evaluating permeabilization techniques and substrate concentrations for Na(+)-K(+)-ATPase measurement at maximum velocity enzyme reaction (Vmax). Terbutaline at 10(-2) M increased enzyme activity, with a maximal response at 15 min that was completely inhibited by 10(-2) M propranolol. This effect of terbutaline was dependent on the presence of serum as well as on the time the cells were in culture. The enhancement of Na(+)-K(+)-ATPase activity was reproduced by 10(-3) M dibutyryl adenosine 3',5'-cyclic monophosphate and 5 x 10(-5) M forskolin. Neither 10(-4) M amiloride nor a sodium-free solution influenced the effect of terbutaline. Western blotting showed that terbutaline did not change the expression of the alpha 1-subunit of the enzyme, which is the predominant form in this cell type. We conclude that beta-adrenergic agonists can modulate Na(+)-K(+)-ATPase activity partially through adenosine 3',5'-cyclic monophosphate and this process is not secondary to an increase in intracellular sodium concentration.w

scholarly journals Involvement of beta1- and beta2- but not beta3-adrenoceptor activation in adrenergic PYY secretion from the isolated colon

2001 ◽  
Vol 168 (1) ◽  
pp. 177-183 ◽  
Author(s):  
S Brechet ◽  
P Plaisancie ◽  
V Dumoulin ◽  
JA Chayvialle ◽  
JC Cuber ◽  
...  
Keyword(s):  
Nervous System ◽  
Adrenergic Receptors ◽  
Hormone Secretion ◽  
Rat Colon ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Adrenergic Blocker ◽  
Beta 2 ◽  
Beta Adrenergic Agonist

The secretion of PYY by endocrine L cells of the terminal gut is under the control of nutrients, the autonomic nervous system and hormones. Catecholamines, and the non-specific beta-adrenergic agonist isoproterenol induce PYY secretion from rat isolated colon or ileum. Because beta3-adrenergic receptors now appear to mediate many of the effects of catecholamines in the gastrointestinal tract, we investigated the involvement of beta1-, beta2-, and beta3-adrenoceptor stimulation in PYY secretion from the isolated, vascularly perfused rat colon. Infusion of 10(-6) M isoproterenol induced a transient increase in PYY secretion (from 36+/-4 to 87+/-20 fmol/2 min; n=7, P<0.05), that was abolished by a previous infusion of the beta1- and beta2-adrenergic blocker (and partial beta3-agonist) alprenolol (10(-6) M). The beta1-adrenergic agonist dobutamine and the beta-2 agonist terbutaline also (both at 10(-5) M) significantly stimulated PYY secretion, from 29+/-1 to 79+/-12 fmol/2 min and from 19+/-1 to 73+/-13 fmol/2 min respectively (n=7, P<0.05). Neither of the beta3-adrenergic agonists tested (BRL 37 344 (10(-5), 10(-6) M) and SR 58 611A (10(-6) M)) significantly stimulated PYY secretion, thus confirming the exclusive involvement of beta1- and beta2-receptors in beta-adrenergic agonist induced hormone secretion.

Effects of isoproterenol on adrenergic constriction in vascular smooth muscle

1977 ◽  
Vol 233 (1) ◽  
pp. H22-H26 ◽  
Author(s):  
S. F. Flaim ◽  
R. Zelis
Keyword(s):  
Smooth Muscle ◽  
Receptor Agonist ◽  
Carotid Arteries ◽  
Constant Pressure ◽  
Adult Rabbit ◽  
Adrenergic Agonist ◽  
Beta Receptors ◽  
Alpha Blockade ◽  
Temperature And Pressure ◽  
Beta Adrenergic Agonist

A series of isolated segments of carotid arteries from Dutch-belted, adult, male rabbits were studied with respect to their response to a beta receptor agonist. Segments of 3-cm length were mounted in a chamber with constant surrounding temperature and pressure and perfused at constant pressure. Inflow pressure, outflow pressure, and flow rate were measured, and values of resistance (R) were calculated. Subsequent to control R, each vessel was exposed to a vasoconstricting concentration of either norepinephrine (NE: 10(-8), 10(-9), 10(-10) M) or potassium (K+: 100mM, 50 mM) followed by three doses of the beta-adrenergic agonist, isoproterenol (IP: 10(-7), 10(-6), 10(-5)M) administered simultaneously with each constrictor. R was not altered by IP during NE infusion but was significantly increased at all levels of IP during both K+ infusions. When the K+ series was repeated with alpha blockade, IP did not alter R. Thus, beta receptors do not appear to be functionally present in the adult rabbit carotid artery.

Catecholamine-fuel interrelationships during exercise in fasting men

1980 ◽  
Vol 48 (1) ◽  
pp. 109-113 ◽  
Author(s):  
J. M. Pequignot ◽  
L. Peyrin ◽  
G. Peres
Keyword(s):  
Maximal Oxygen Consumption ◽  
Plasma Catecholamines ◽  
Plasma Free Fatty Acid ◽  
Work Load ◽  
Bicycle Ergometer ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Adrenergic Response ◽  
Response To Exercise

Adrenergic response to exercise and the relationships between plasma catecholamines and blood energetic substrates were studied in sedentary men after 15 h of fasting. Subjects pedaled a bicycle ergometer until exhaustion at a work load approximating 80% maximal oxygen consumption. Working ability was diminished by the fast (P less than 0.025). Resting plasma norepinephrine level was increased by fasting. During exercise plasma epinephrine (E) and norepinephrine (NE) concentrations were more elevated in fasting subjects than in fed subjects. Plasma catecholamine (CA) levels in fasting men correlated with blood glucose, blood lactate, and plasma glycerol concentrations. There was no significative correlation between CA and plasma free fatty acid (FFA) levels. The increased adrenergic activity in fasting subjects correlated with reduced endurance time. This study emphasizes the role of CA release, probably combined with other hormonal factors, in the mobilization of energy substrates during submaximal exercise.

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