The effect of β-adrenergic agonists on the membrane potential of fat-cell mitochondria in situ

1. The accumulation of [3H]methyltriphenylphosphonium by isolated fat-cells was used to estimate the membrane potential of mitochondria in situ. 2. Adrenaline caused a large decrease in the accumulation of [3H]methyltriphenylphosphonium. Mitochondria in fat-cells incubated in the presence of adrenaline had a very low calculated membrane potential. This effect was also given by isoprenaline (a beta-adrenergic agonist) and was blocked by propranolol (a beta-adrenergic antagonist). 3. The effect of isoprenaline could be partially antagonized by the use of media with high albumin concentrations. Addition of sodium oleate to saturate the fatty acid-binding sites on the albumin reversed this antagonism. 4. It is proposed that the decrease in the calculated mitochondrial membrane potential is due to the uncoupling effect of the non-esterified fatty acids released by the stimulation of lipolysis observed in the presence of beta-adrenergic agonists.

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Effect of adrenergic agonists on big and small renin

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1980.238.5.e416 ◽

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.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.261.5.h1499 ◽

1991 ◽

Vol 261 (5) ◽

pp. H1499-H1507 ◽

Cited By ~ 4

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.

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

Canadian Journal of Animal Science ◽

10.4141/cjas92-002 ◽

1992 ◽

Vol 72 (1) ◽

pp. 15-21 ◽

Cited By ~ 7

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

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Modulation of in situ canine intrinsic cardiac neuronal activity by nicotinic, muscarinic, and beta-adrenergic agonists

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.265.3.r659 ◽

1993 ◽

Vol 265 (3) ◽

pp. R659-R669 ◽

Cited By ~ 7

Author(s):

M. H. Huang ◽

F. M. Smith ◽

J. A. Armour

Keyword(s):

Neuronal Activity ◽

Adrenergic Receptors ◽

Neuronal Responses ◽

Adrenergic Agonists ◽

Beta Adrenergic Receptors ◽

Beta Adrenergic ◽

Beta Adrenergic Agonists ◽

Anesthetized Dogs ◽

Bethanechol Chloride

To investigate whether microvolumes (< or = 10 microliters) of nicotinic, muscarinic, and beta-adrenergic agonists can modify intrinsic cardiac neuronal activity, nicotine, 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), bethanechol chloride, and isoproterenol were separately administered adjacent to spontaneously active in situ epicardial neurons in 15 anesthetized dogs. Neuronal activity generated by 46 of 63 neurons was modified by these neurochemicals, with about half of the neurons affected by more than one agent. In association with these neuronal responses, cardiodynamic responses were elicited in 17 instances. When cardiac augmentation was elicited, it persisted after the administration of atropine but not of timolol. After cardiac decentralization, 40% of previously active neurons were still modified by local application of chemicals; cardiodynamic responses were elicited in nine instances. The activity of six units was modified by isoproterenol after subsequent administration of hexamethonium. These data confirm that intrinsic cardiac neurons possess nicotinic and muscarinic receptors and demonstrate that some intrinsic cardiac neurons also possess beta-adrenergic receptors. Furthermore, these data demonstrate that intrinsic cardiac neurons with nicotinic, muscarinic, and beta-adrenergic receptors are involved in cardiac regulation.

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Beta-adrenergic inhibition of Na-K-Cl cotransport in lymphocytes

AJP Cell Physiology ◽

10.1152/ajpcell.1992.263.5.c1015 ◽

1992 ◽

Vol 263 (5) ◽

pp. C1015-C1020 ◽

Cited By ~ 4

Author(s):

R. D. Feldman

Keyword(s):

Physiological Role ◽

Lymphocyte Function ◽

Beta Adrenergic ◽

Homogeneous Population ◽

Beta Adrenoceptor ◽

Beta Adrenergic Agonists ◽

Adrenergic Antagonist ◽

Human Lymphoma ◽

Extracellular Sodium ◽

Beta Adrenergic Agonist

Lymphocytes contain a homogeneous population of beta 2-adrenoceptors. However, their physiological role in the regulation of lymphocyte function, especially early in the activation/proliferation process, remains unclear. To study the role of beta-adrenergic activation on the regulation of membrane transport, we examined 86Rb uptake in the Jurkat human lymphoma cell line. 86Rb uptake was predominantly accounted for by bumetanide-sensitive uptake (74 +/- 2% total 86Rb uptake) and ouabain-sensitive uptake (20 +/- 2%). Bumetanide potently inhibited 86Rb uptake (50% inhibitory concentration = 210 +/- 40 nM), and bumetanide-sensitive uptake was dependent on extracellular sodium and chloride, consistent with uptake via Na-K-Cl cotransport. The beta-adrenergic agonist isoproterenol (10 microM) mediated a 50 +/- 11% reduction in bumetanide-sensitive uptake without a significant alteration in ouabain-sensitive uptake. The effect of isoproterenol was potent (50% effective concentration = 4.42 +/- 1.70 nM), stereoselective, and was inhibited by the beta-adrenergic antagonist nadolol. The effect of isoproterenol was mimicked by permeant adenosine 3',5'-cyclic monophosphate analogues but not by pindolol. These data indicate that beta-adrenoceptor activation decreases 86Rb uptake in lymphocytes via inhibition of Na-K-Cl cotransport. Modulation of this transporter could be one mechanism by which beta-adrenergic agonists regulate lymphocyte function.

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

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1995.268.6.l983 ◽

1995 ◽

Vol 268 (6) ◽

pp. L983-L990 ◽

Cited By ~ 17

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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The effect of α-adrenergic agonists on the membrane potential of fat-cell mitochondria in situ

Biochemical Journal ◽

10.1042/bj2060619 ◽

1982 ◽

Vol 206 (3) ◽

pp. 619-626 ◽

Cited By ~ 4

Author(s):

R J Davis ◽

B R Martin

Keyword(s):

Membrane Potential ◽

Mitochondrial Membrane Potential ◽

Adrenergic Receptor ◽

Mitochondrial Membrane ◽

Fat Cell ◽

Alpha Adrenergic Receptor ◽

Low Concentrations ◽

Adrenergic Antagonist ◽

Potency Order

1. The accumulation of [3H]methyltriphenylphosphonium by isolated fat-cells was used to estimate the membrane potential of mitochondria in situ. 2. An alpha-adrenergic receptor-mediated decrease in the apparent accumulation of [3H]methyltriphenylphosphonium was observed. Methoxamine, clonidine and low concentrations of phenylephrine decreased the calculated mitochrondrial membrane potential without significantly raising cyclic AMP levels, adenylate cyclase activity or stimulating lipolysis. The agonist potency order was phenylephrine greater than methoxamine greater than clonidine. 3. The decrease in the calculated mitochondrial membrane potential caused by phenylephrine, clonidine and methoxamine was blocked by the alpha-adrenergic antagonist prazosin but not by yohimbine nor by the beta-antagonist propranolol. This suggests that the effect on the calculated mitochondrial membrane potential may be mediated by alpha 1-like receptors.

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