scholarly journals Stable changes to calcium fluxes in mitochondria isolated from rat livers perfused with α-adrenergic agonists and with glucagon

1980 ◽  
Vol 188 (2) ◽  
pp. 443-450 ◽  
Author(s):  
Wayne M. Taylor ◽  
Veronica Prpić ◽  
John H. Exton ◽  
Fyfe L. Bygrave
Keyword(s):  
Adenine Nucleotides ◽  
Calcium Content ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Short Term ◽  
Adrenergic Antagonist ◽  
Prolonged Retention ◽  
Nadph Oxidation ◽  
Reduced Rate ◽  
Rat Livers

Mitochondria isolated from rat liver after a short-term perfusion with the α-adrenergic agonist phenylephrine or with glucagon exhibited enhanced rates of uptake of Ca2+ and prolonged retention of Ca2+ in the presence of 4mm-Pi. The effect of Ca2+ retention was apparent after perfusion with phenylephrine for only 1min and was maximal after 7min of treatment. The changes induced by glucagon, although similar, were less rapid. Adrenaline caused similar changes to phenylephrine and its effects were blocked by the α-adrenergic antagonist phenoxybenzamine, but not by the β-antagonist propranolol. The Ca2+ content of the isolated mitochondria decreased by 30% 1min after the onset of perfusion with phenylephrine; by 6min it had begun to return to the original value which was reached at 10min. A similar loss in calcium content was induced by glucagon but the changes were not as great and occurred more slowly. Mitochondria from phenylephrine-treated livers exhibited decreased rates of Ca2+ efflux induced by addition of 2mm-EGTA, a 50% increase in the contents of ADP and total adenine nucleotides, a small increase in the transmembrane pH gradient, and a reduced rate of oxaloacetate-induced NADPH oxidation. This study thus shows that stimulation of liver by α-adrenergic agonists, like that by glucagon, induces within minutes a stable modification of mitochondria leading to alterations in the Ca2+-translocation cycle (increased Ca2+ uptake and retention) and alterations in mitochondrial energy-linked reactions.

scholarly journals Determination of mitochondrial calcium content in hepatocytes by a rapid cellular-fractionation technique. α-adrenergic agonists do not mobilize mitochondrial Ca2+

1984 ◽  
Vol 219 (2) ◽  
pp. 383-389 ◽  
Author(s):  
S B Shears ◽  
C J Kirk
Keyword(s):  
Glycogen Phosphorylase ◽  
Preceding Paper ◽  
Calcium Content ◽  
Total Cell ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Energy Dependent ◽  
Glycogen Phosphorylase Activity ◽  
Alpha Adrenergic Agonist

A rapid cellular fractionation technique [the preceding paper, Shears & Kirk (1984) Biochem. J., 219, 375-382] was employed to separate a mitochondria-rich fraction from hepatocytes within seconds. Mitochondrial Ca was estimated to be no more than 41% of total cell Ca. At least half of the mitochondrial Ca was present in an energy-dependent pool; 20% of total cell Ca was accessible to EGTA within 10s. The alpha-adrenergic agonist phenylephrine stimulated glycogen phosphorylase activity by 100% within 0.5 min and induced a loss of 20% of total cell Ca after 10 min from the EGTA-inaccessible pool. However, between 0.5 and 10 min after the addition of phenylephrine to hepatocytes there was no significant change in the Ca content of the mitochondria-rich fraction. Hepatocytes that were preloaded with Ca2+ during 90 min incubation at 0-4 degrees C expelled this cation during 20 min incubation at 37 degrees C. After this time, phenylephrine failed to alter the Ca content of a mitochondria-rich fraction. It is concluded that alpha-adrenergic agonists do not mobilize Ca2+ from hepatocyte mitochondria.

Denopamine, a β1-adrenergic agonist, increases alveolar fluid clearance in ex vivo rat and guinea pig lungs

2001 ◽  
Vol 90 (1) ◽  
pp. 10-16 ◽  
Author(s):  
Tsutomu Sakuma ◽  
Chiharu Tuchihara ◽  
Masanobu Ishigaki ◽  
Kazuhiro Osanai ◽  
Yoshihiro Nambu ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Ex Vivo ◽  
Progressive Increase ◽  
Alveolar Type ◽  
Dependent Manner ◽  
Alveolar Fluid Clearance ◽  
Adrenergic Agonist ◽  
Short Term ◽  
Adrenergic Antagonist ◽  
Dose Dependent

The effect of denopamine, a selective β1-adrenergic agonist, on alveolar fluid clearance was determined in both ex vivo rat and guinea pig lungs. Alveolar fluid clearance was measured by the progressive increase in the concentration of Evans blue-labeled albumin over 1 h at 37°C. Denopamine (10−6 to 10−3 M) increased alveolar fluid clearance in a dose-dependent manner in ex vivo rat lungs. Denopamine also stimulated alveolar fluid clearance in guinea pig lungs. Atenolol, a selective β1-adrenergic antagonist, and amiloride, a sodium channel inhibitor, inhibited denopamine-stimulated alveolar fluid clearance. The potency of denopamine was similar to that of similar doses of isoproterenol or terbutaline. Short-term hypoxia (100% nitrogen for 1–2 h) did not alter the stimulatory effect of denopamine. Denopamine (10−4, 10−3 M) increased intracellular adenosine 3′,5′-cyclic monophosphate levels in cultured rat alveolar type II cells. In summary, denopamine, a selective β1-adrenergic agonist, stimulates alveolar fluid clearance in both ex vivo rat and guinea pig lungs.

Predominantly beta-adrenergic control of equine sweating

1984 ◽  
Vol 246 (3) ◽  
pp. R349-R353 ◽  
Author(s):  
J. Bijman ◽  
P. M. Quinton
Keyword(s):  
Sweat Glands ◽  
Maximal Response ◽  
Exocrine Glands ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Sweat Secretion ◽  
Adrenergic Antagonist ◽  
Adrenergic Control

Single equine sweat glands were found to secrete for more than 1 h in vitro in response to pharmacologic secretagogues. The adrenergic agonists epinephrine and norepinephrine evoked maximal sweat rates of 2.0 nl X gland-1 X min-1. However, the concentration of norepinephrine (10(-5) M) required to evoke the maximal response was 10 times higher than that for epinephrine. Maximal sweat rates also were stimulated with the beta 2-adrenergic agonist terbutaline. This stimulation was blocked by the beta-adrenergic antagonist propranolol. Moderate sweating responses were also obtained with the alpha-adrenergic agonists phenylephrine and methoxamine, but these responses also were blocked by propranolol. Neither the muscarinic blocker atropine nor the alpha-adrenergic antagonist phentolamine inhibited any of the pharmacologically induced sweat responses. Unlike most other mammalian exocrine glands, cholinergic agonists were ineffective in stimulating sweat secretion. Therefore equine sweat glands apparently are under predominantly beta-adrenergic control.

Evidence for α-adrenergic receptors acting through the guanylate cyclase system in human cultured thyroid cells

1983 ◽  
Vol 104 (1) ◽  
pp. 64-68 ◽  
Author(s):  
Maria Luisa Brandi ◽  
Carlo M. Rotella ◽  
Annalisa Tanini ◽  
Roberto S. Toccafondi
Keyword(s):  
Guanylate Cyclase ◽  
Adrenergic Receptors ◽  
Human Thyroid ◽  
Camp Accumulation ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Thyroid Cells ◽  
Camp Content ◽  
Adrenergic Antagonist ◽  
Camp Levels

Abstract. In order to investigate the presence of α-adrenergic receptors in human thyroid, we have studied the effect of α-adrenergic agonists and antagonists on cGMP cellular content of human thyroid cells in primary culture. Epinephrine as well as TSH were not able to modify the cGMP cellular levels, while norepinephrine significantly increased cGMP accumulation already at 10 nm, a dose inactive on cAMP accumulation. A non selective α-adrenergic antagonist, phentolamine, significantly inhibited cGMP accumulation induced by norepinephrine. Norepinephrine-induced cGMP accumulation was unaffected by prazosin, an α1-adrenergic antagonist, but was abolished by yohimbine, an α2-adrenergic antagonist. Phenylephrine, an α-adrenergic agonist, produced an increase of cellular cGMP levels without modifying cAMP content. In the presence of TSH, the cGMP response to norepinephrine was not modified; however, the increase of cAMP levels was inhibited by norepinephrine at doses inactive on cAMP accumulation, but active on cGMP levels. The present results demonstrate the existence in human thyroid cells of α2-adrenergic receptors, regulating the guanylate cyclase system. It may be postulated that the counter-regulation exerted by α-adrenergic agonists on the response to TSH operates on the TSH-dependent adenylate cyclase.

Impact of β-adrenergic agonist on Na+ channel and Na+-K+-ATPase expression in alveolar type II cells

1998 ◽  
Vol 275 (2) ◽  
pp. L414-L422 ◽  
Author(s):  
Yoshiaki Minakata ◽  
Satoshi Suzuki ◽  
Czeslawa Grygorczyk ◽  
André Dagenais ◽  
Yves Berthiaume
Keyword(s):  
Gene Expression ◽  
Atpase Activity ◽  
Continuous Treatment ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Short Term ◽  
Alveolar Type Ii Cells

It has been shown that short-term (hours) treatment with β-adrenergic agonists can stimulate lung liquid clearance via augmented Na+ transport across alveolar epithelial cells. This increase in Na+ transport with short-term β-agonist treatment has been explained by activation of the Na+ channel or Na+-K+-ATPase by cAMP. However, because the effect of sustained stimulation (days) with β-adrenergic agonists on the Na+ transport mechanism is unknown, we examined this question in cultured rat alveolar type II cells. Na+-K+-ATPase activity was increased in these cells by 10−4 M terbutaline in an exposure time-dependent manner over 7 days in culture. This increased activity was also associated with an elevation in transepithelial current that was inhibited by amiloride. The enzyme’s activity was also augmented by continuous treatment with dibutyryl-cAMP (DBcAMP) for 5 days. This increase in Na+-K+-ATPase activity by 10−4 M terbutaline was associated with an increased expression of α1-Na+-K+-ATPase mRNA and protein. β-Adrenergic agonist treatment also enhanced the expression of the α-subunit of the epithelial Na+ channel (ENaC). These increases in gene expression were inhibited by propranolol. Amiloride also suppressed this long-term effect of terbutaline and DBcAMP on Na+-K+-ATPase activity. In conclusion, β-adrenergic agonists enhance the gene expression of Na+-K+-ATPase, which results in an increased quantity and activity of the enzyme. This heightened expression is also associated with augmented ENaC expression. Although the cAMP system is involved, the inhibition of enhanced enzyme activity with amiloride suggests that increased Na+ entry at the apical surface plays a role in this process.

Peripheral progesterone concentrations in the luteal-phase ewe: effects of a β-adrenergic receptor antagonist and two β2-adrenergic agonists

1988 ◽  
Vol 116 (1) ◽  
pp. 137-142 ◽  
Author(s):  
A. G. Wheeler ◽  
J. Lean ◽  
M. Walker
Keyword(s):  
Luteal Phase ◽  
Sympathetic Innervation ◽  
Physiological Role ◽  
Adrenergic Agonists ◽  
Progesterone Concentration ◽  
Adrenergic Agonist ◽  
Arterial Blood ◽  
Experimental Drug ◽  
Adrenergic Antagonist ◽  
Conscious Sheep

ABSTRACT Peripheral blood samples were collected at 10-min intervals from three conscious sheep in which ovulation had been induced 6–10 days previously using exogenous hormones. Saline was infused into a jugular vein for about 1 h, followed by the experimental drug for 1–2 h and followed by saline again for a further 2 h. The experiments were repeated following induced luteolysis and ovulation. The infusion of a β-adrenergic antagonist (propranolol) into three conscious luteal-phase ewes decreased (P<0·05) the peripheral progesterone concentration in each animal. Infusions of β2-adrenergic agonists (ritodrine and salbutamol) increased (P<0·05) the progesterone concentration in four out of eight experiments. The β-adrenergic antagonist decreased the heart rate and the β2-adrenergic agonist increased it; the arterial blood pressure and respiratory rate were unaffected. The decrease in the prosgesterone concentration in response to the β-adrenergic antagonist suggests that the normal ovarian secretion of progesterone is partly the result of sympathetic stimulation, and that the sympathetic innervation of the ovary may have a physiological role in modulating progesterone secretion. J. Endocr. (1988) 116, 137–142

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.

Effects of endogenous and exogenous catecholamines on LPS-induced neutrophil trafficking and activation

1999 ◽  
Vol 276 (1) ◽  
pp. L1-L8 ◽  
Author(s):  
Edward Abraham ◽  
Debra J. Kaneko ◽  
Robert Shenkar
Keyword(s):  
Systemic Circulation ◽  
Mrna Levels ◽  
Adrenergic Stimulation ◽  
Neutrophil Accumulation ◽  
Adrenergic Agonist ◽  
Nitric Oxide Synthase Inhibitor ◽  
Adrenergic Agents ◽  
Adrenergic Antagonist ◽  
Tnf Α ◽  
Synthase Inhibitor

Endotoxemia produces elevations in catecholamine levels in the pulmonary and systemic circulation as well as rapid increases in neutrophil number and proinflammatory cytokine expression in the lungs. In the present experiments, we examined the effects of endogenous and exogenous adrenergic stimulation on endotoxin-induced lung neutrophil accumulation and activation. Levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and macrophage inflammatory protein (MIP)-2 mRNAs were increased in lung neutrophils from endotoxemic mice compared with those present in lung neutrophils from control mice or in peripheral blood neutrophils from endotoxemic or control mice. Treatment with the β-adrenergic antagonist propranolol before endotoxin administration did not affect trafficking of neutrophils to the lungs or the expression of IL-1β, TNF-α, or MIP-2 by lung neutrophils. Administration of the α-adrenergic antagonist phentolamine before endotoxemia did not alter lung neutrophil accumulation as measured by myeloperoxidase (MPO) levels but did result in significant increases in IL-1β, TNF-α, and MIP-2 mRNA expression by lung neutrophils compared with endotoxemia alone. Administration of the α1-adrenergic agonist phenylephrine before endotoxin did not affect trafficking of neutrophils to the lungs but was associated with significantly increased expression of TNF-α and MIP-2 mRNAs by lung neutrophils compared with that found after endotoxin alone. In contrast, treatment with the α2-adrenergic agonist UK-14304 prevented endotoxin-induced increases in lung MPO and lung neutrophil cytokine mRNA levels. The suppressive effects of UK-14304 on endotoxin-induced increases in lung MPO were not affected by administration of the nitric oxide synthase inhibitor N-nitro-l-arginine methyl ester. These data demonstrate that the initial accumulation and activation of neutrophils in the lungs after endotoxemia can be significantly diminished by α2-adrenergic stimulation. Therapy with α2-adrenergic agents may have a role in modulating inflammatory pulmonary processes associated with sepsis-induced acute lung injury.

Dual α2-Adrenergic Agonist and α1-Adrenergic Antagonist Actions of Dexmedetomidine on Human Isolated Endothelium-Denuded Gastroepiploic Arteries

2002 ◽  
Vol 94 (6) ◽  
pp. 1434-1440 ◽  
Author(s):  
Junichirou Hamasaki ◽  
Isao Tsuneyoshi ◽  
Rumi Katai ◽  
Tatewaki Hidaka ◽  
Walter A. Boyle ◽  
...  
Keyword(s):  
Adrenergic Agonist ◽  
Adrenergic Antagonist
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