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.

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.

Effects of beta-adrenergic agonists on splanchnic vascular volume and cardiac output

1991 ◽  
Vol 261 (5) ◽  
pp. H1499-H1507 ◽  
Author(s):  
P. I. Chang ◽  
D. L. Rutlen
Keyword(s):  
Cardiac Output ◽  
Adrenergic Agonists ◽  
Beta Adrenergic ◽  
Splenic Volume ◽  
Alpha Adrenoceptor ◽  
Beta Adrenergic Agonists ◽  
Anesthetized Dogs ◽  
Beta 2 ◽  
Beta Adrenergic Agonist ◽  
Adrenergic Effects

The effect of beta-adrenergic agonists on splanchnic intravascular volume (SIV), measured with radionuclide imaging, and the subsequent influence of such volume changes on cardiac output (CO) were examined in 40 anesthetized dogs. Isoproterenol (6 micrograms/min) caused a decrease in total SIV of 12 +/- 1% (P less than 0.001). The decrease was due entirely to a decrease in splenic volume of 24 +/- 3% (P less than 0.001), since volume increased in the remainder of the splanchnic vasculature [hepatic and mesenteric volume increased 12 +/- 2% (P less than 0.001) and 11 +/- 3% (P less than 0.02), respectively]. CO increased from 1,724 +/- 187 to 3,138 +/- 321 ml/min (P less than 0.001); after subsequent splenectomy, isoproterenol caused a similar increment. Isoproterenol-associated SIV changes were not altered by carotid denervation and vagotomy or by beta 1-adrenergic inhibition with metoprolol but were abolished by nonselective beta-adrenergic inhibition with propranolol. With a larger dose of metoprolol and smaller dose of isoproterenol to minimize beta 1-adrenergic effects, the isoproterenol-associated CO increment was attenuated (P less than 0.01) by splenectomy. With the beta 2-agonist terbutaline (41 micrograms/min) after metoprolol, total SIV decreased 15 +/- 4% (P less than 0.001). After subsequent alpha-adrenergic inhibition with phenoxybenzamine, terbutaline caused no change in SIV and an attenuated (P less than 0.05) increase in CO. Thus beta-adrenergic agonist administration causes a decrease in total SIV due entirely to a decrease in splenic volume. The SIV decrement is dependent on beta 2- and alpha-adrenoceptor stimulation and appears to enhance CO only if beta 1-adrenergic effects are minimized.

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

Characterization of beta-adrenoreceptors on smooth muscle cells from guinea pig stomach

1990 ◽  
Vol 259 (3) ◽  
pp. G436-G442
Author(s):  
L. Zhang ◽  
R. T. Jensen ◽  
P. N. Maton
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Adrenergic Receptors ◽  
Muscle Cells ◽  
Adrenergic Agonists ◽  
Beta Adrenergic ◽  
Gastric Smooth Muscle ◽  
Ici 118,551 ◽  
Beta 2 ◽  
Relative Potencies

To characterize the beta-adrenergic receptors on guinea pig gastric smooth muscle cells, we examined the effects of beta-adrenergic agonists and antagonists on biological activity, cellular adenosine 3',5'-cyclic monophosphate (cAMP), and radioligand binding. Adrenergic agonists, isoproterenol (ISO), epinephrine (EPI), and norepinephrine (NE), inhibited carbachol-stimulated contraction of muscle cells, with relative potencies (IC50S) of ISO (0.1 microM) greater than EPI (1.4 microM) greater than NE (11 microM). Each agonist increased cellular cAMP, with relative potencies (IC50S) of ISO (0.5 microM) greater than EPI (6.3 microM) greater than NE (56 microM). Binding of the nonselective beta-antagonist 125I-pindolol was temperature-dependent, saturable, reversible, and specific. 125I-pindolol binding was inhibited by the three agonists, with relative potencies (IC50S) of ISO (0.9 microM) greater than EPI (9.6 microM) greater than NE (112 microM). Pindolol inhibited binding of 125I-pindolol with an IC50 of 100 nM. The IC50 for inhibition of binding of 125I-pindolol by the relatively beta 2-selective antagonist ICI 118,551 was 70 nM and for the relatively beta 1-selective antagonist betaxolol was 1,000 nM. Computer analysis of the dose-inhibition curves for binding of 125I-pindolol for the antagonists indicated that gastric smooth muscle cells possess exclusively beta 2-adrenergic receptors of two classes, one class with a high affinity for ICI 118,551 (Kd = 50 nM) and the other with a low affinity for ICI 118,551 (Kd = 30 microM). Our results indicate that beta-adrenergic agonists interact with beta 2-adrenergic receptors on gastric smooth muscle cells to increase cellular cAMP and inhibit muscle contraction.

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.

scholarly journals Comparative effect of glucagon and isoproterenol on hepatic glycogenolysis and glycolysis in isolated perfused liver

2003 ◽  
Vol 46 (4) ◽  
pp. 563-568 ◽  
Author(s):  
Márcia Vardanega-Peicher ◽  
Ricardo Galletto ◽  
Sarah Pagliarini e Silva ◽  
Roberto Barbosa Bazotte
Keyword(s):  
Adrenergic Receptors ◽  
Perfused Liver ◽  
Beta Adrenergic Receptors ◽  
Adrenergic Agonist ◽  
Comparative Effect ◽  
Beta Adrenergic ◽  
Isolated Perfused Liver ◽  
Maximal Activation ◽  
Inhibition Of Glycolysis ◽  
Beta Adrenergic Agonist

The effect of glucagon and isoproterenol (beta-adrenergic agonist) on hepatic glycogenolysis and glycolysis in isolated perfused liver was compared. The levels of isoproterenol and glucagon which promoted the maximal activation of glycogenolysis were 20 muM and 1nM respectively. However, glucagon (1 nM) not only increased glycogenolysis but also inhibited glycolysis. Because adenosine-3'-5'-cyclic monophosphate (cAMP) is a common second messenger to glucagon and isoproterenol, the level of cAMP that simulates the effect of these substances were investigated. The concentration of cAMP that inhibited glycolysis was five times higher (15 muM) than that which stimulated glycogenolysis (3 muM). Similar inhibition of glycolysis was obtained with cAMP agonists resistant to phosphodiesterases, i.e., 8-Br-cAMP and N6-monobutyryl-cAMP (6-MB-cAMP) at the concentration of 3 muM. Thus, apparently glucagon could produce higher cellular levels of cAMP than that obtained with the activation of beta-adrenergic receptors. The higher amount of cAMP could be enough to overcome the action of phosphodiesterases and penetrate in the cytosol creating a favourable gradient to inhibit the enzymes of glycolysis.

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

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