scholarly journals Metabolic effect of α-and the β-adrenergic stimulation of rat submaxillary gland in vitro

1976 ◽  
Vol 160 (3) ◽  
pp. 597-601 ◽  
Author(s):  
M P Thompson ◽  
D H Williamson
Keyword(s):  
Submaxillary Gland ◽  
Metabolic Effect ◽  
Metabolic Responses ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Presence And Absence ◽  
Stimulation Of

1. Incubation of submaxillary-gland slices with isoproterenol, a β-adrenergic agonist, stimulated glucose removal by 41% and decreased tissue [glucose 6-phosphate] by 50%. Propranolol blocked these effects of isoproterenol. 2. Phenylephrine, an α-adrenergic agonist, stimulated glucose removal by 35% and decreased tissue [glucose 6-phosphate] by 75%. In addition, phenylephrine also completely overcame the inhibition of pyruvate removal caused by acetoacetate metabolism and decreased tissue [atp] by 45%. Phentolamine blocked the effects of phenylephrine. 3. In contrast with β-adrenergic stimulation, α-adrenergic stimulation required exogenous Ca2+. 4. These results explain the different metabolic responses of the submaxillary gland to adrenaline in the presence and absence of exogenous Ca2+.

Regulation of ciliary beat frequency by autonomic mechanisms: in vitro

1988 ◽  
Vol 65 (4) ◽  
pp. 1895-1901 ◽  
Author(s):  
L. B. Wong ◽  
I. F. Miller ◽  
D. B. Yeates
Keyword(s):  
Laser Light ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Atropine Sulfate ◽  
Adrenergic Agonist ◽  
Muscarinic Cholinergic ◽  
Autonomic Receptors ◽  
Stimulation Of ◽  
Ciliary Beat

The ciliated epithelium of the mammalian trachea separates the neurohumoral milieu of the tissue from that of the environment of the airway lumen. To determine whether specific autonomic receptors regulating ciliary beat frequency (CBF) were located on mucosal or serosal sides, we measured CBF by heterodyne mode correlation analysis laser light scattering in bovine tracheal tissues mounted in a two-sided chamber. A beta 2-adrenergic agonist, fenoterol, at 10(-7) M, stimulated serosal CBF from 7.9 +/- 1.3 to 20.2 +/- 5.8 Hz (P less than 0.01) and mucosal CBF from 6.6 +/- 0.9 to 14.7 +/- 4.6 Hz (P less than 0.01). A muscarinic cholinergic agonist, methacholine, at 10(-7) M, increased mucosal CBF from 8.4 +/- 1.0 to 19.5 +/- 5.5 Hz (P less than 0.01) and serosal CBF from 8.0 +/- 0.9 to 15.4 +/- 5.0 Hz (P less than 0.01). The differences in stimulation of CBF on the mucosal and serosal sides between fenoterol and methacholine were significant (P less than 0.01). Studies in which these autonomic agonist stimulating effects were inhibited by their respective antagonists, propranolol and atropine sulfate, demonstrated that CBF can be regulated independently by mediators both in the submucosa and within the mucus lining.

UPTAKE OF ALDOSTERONE BY HUMAN SKIN AND STIMULATION OF RNA SYNTHESIS IN THE SWEAT GLAND IN VITRO

1969 ◽  
Vol 45 (2) ◽  
pp. 231-NP ◽  
Author(s):  
K. DIXON ◽  
V. SCHWARZ
Keyword(s):  
Human Skin ◽  
Sweat Gland ◽  
Rna Synthesis ◽  
Sweat Duct ◽  
Large Excess ◽  
Receptor Sites ◽  
Presence And Absence ◽  
Stimulation Of

SUMMARY Autoradiography of human skin, after incubation with tritiated aldosterone or pregnenolone, showed both steroids to be concentrated in all types of cells. Binding of [3H]aldosterone in skin was investigated in the presence and absence of a large excess of unlabelled hormone. The capacity of the cells to bind aldosterone in a manner suggesting attachment to receptor sites was estimated to be 5 × 10-13 moles/g. The rate of RNA synthesis was measured in the various cells of the sweat gland: it was shown to be significantly increased by aldosterone. This stimulation was observed in the inner and outer cells of the sweat duct and probably also in the secretory tubule.

Regulation of lipolysis by somatotropin: functional alteration of adrenergic and adenosine signaling in bovine adipose tissue

1997 ◽  
Vol 152 (3) ◽  
pp. 465-475 ◽  
Author(s):  
K L Houseknecht ◽  
D E Bauman
Keyword(s):  
Adipose Tissue ◽  
Signaling Proteins ◽  
Heterotrimeric G Proteins ◽  
Adrenergic Stimulation ◽  
Cellular Mechanisms ◽  
Lactating Cows ◽  
Adipose Tissue Lipolysis ◽  
Stimulation Of

To investigate the cellular mechanisms of somatotropin (ST) action on adipose tissue lipolysis, experiments were conducted using adipose tissue taken from lactating cows treated with excipient or ST (40 mg/day). Stimulation of lipolysis in vitro by the effectors isoproterenol with or without adenosine deaminase, dibutyryl cAMP with or without isobutylmethylxanthine, and forskolin was not altered by ST treatment. Conversely, the response to the antilipolytic effector, phenylisopropyladenosine (PIA), was significantly reduced in adipose tissue explants from ST or fasted cows. The different responses to adrenergic-stimulating agents (in vivo) and PIA (in vitro) were not due to differences in the abundance of α, β or γ subunits of the stimulatory (Gs) and inhibitory (Gi) subunits of the heterotrimeric G-proteins which bind to the β-adrenergic and adenosine receptors respectively. However, the functionality of Gi proteins, as assessed by their ability to be ADP-ribosylated by pertussis toxin, was significantly reduced in ST-treated but not fasted cows. These data highlight differential regulation of signaling proteins by ST and fasting, both of which result in enhanced in vivo response to adrenergic stimulation of lipolysis. Journal of Endocrinology (1997) 152, 465–475

scholarly journals NCLX prevents cell death during adrenergic activation of the brown adipose tissue

2018 ◽  
Author(s):  
Essam A. Assali ◽  
Anthony E. Jones ◽  
Michaela Veliova ◽  
Mahmoud Taha ◽  
Nathanael Miller ◽  
...  
Keyword(s):  
Cell Death ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Mitochondrial Permeability Transition ◽  
Core Body Temperature ◽  
Adrenergic Stimulation ◽  
Brown Adipose ◽  
Stimulation Of

AbstractA sharp increase in mitochondrial Ca2+ marks the activation of the brown adipose tissue (BAT) thermogenesis, yet the mechanisms preventing Ca2+ deleterious effects are poorly understood. Here, we show that adrenergic stimulation of BAT activates a PKA-dependent mitochondrial Ca2+ extrusion via the mitochondrial Na+/Ca2+ exchanger, NCLX. Adrenergic stimulation of NCLX-ablated brown adipocytes (BA) induces a profound mitochondrial Ca2+ overload and impaired uncoupled respiration. Core body temperature, PET imaging and VO2 measurements confirm a BAT specific thermogenic defect in NCLX-null mice.We show that mitochondrial Ca2+ overload induced by adrenergic stimulation of NCLX-null BAT, triggers the opening of the mitochondrial permeability transition pore (mPTP), leading to remarkable mitochondrial swelling, Cytochrome c release and cell death in BAT. However, treatment with mPTP inhibitors rescue mitochondrial respiratory function and thermogenesis in NCLX-null BA, in vitro and in vivo.Our findings identify a novel pathway enabling non-lethal mitochondrial Ca2+ elevation during adrenergic stimulation of uncoupled respiration. Deletion of NCLX transforms the adrenergic pathway responsible for the stimulation of thermogenesis into a death pathway.

scholarly journals Metabolic-membrane coupling in red blood cells of trout: the effects of anoxia and adrenergic stimulation

1989 ◽  
Vol 143 (1) ◽  
pp. 149-164 ◽  
Author(s):  
R. A. Ferguson ◽  
R. G. Boutilier
Keyword(s):  
Blood Cells ◽  
Energy Production ◽  
Red Cells ◽  
Salmo Gairdneri ◽  
Red Cell ◽  
Adrenergic Stimulation ◽  
Tight Coupling ◽  
Metabolic Coupling ◽  
Stimulation Of

Under oxygenated conditions, in vitro, the highly aerobic red cells of the rainbow trout (Salmo gairdneri) exhibit tight coupling between energy (i.e. nucleotide triphosphate, NTP)-consuming and NTP-producing metabolic activity, as shown by strict maintenance of red cell NTP:haemoglobin ratios. This coupling is maintained following adrenergic stimulation of oxygenated red cells when the increased NTP demands of ion transporting systems are met by enhanced energy production via aerobic metabolism. In unstimulated anoxic red cells, membrane-metabolic coupling is preserved via the arrest of NTP-consuming processes. Adrenergic stimulation of anoxic red cells, however, leads to a functional uncoupling of membrane metabolism with the result that NTP levels decline rapidly. At this time, cellular [NTP] is negatively correlated with [Na+]i and [Cl-]i and positively correlated with [K+]i. This, in addition to the fact that the pH of the intracellular compartment is also highly dependent on cellular NTP levels, provides evidence for the integration of energy and membrane metabolisms.

Adrenergic stimulation of glycolysis without change in glycolytic enzyme binding in rainbow trout (Oncorhynchus mykiss) erythrocytes

1994 ◽  
Vol 72 (5) ◽  
pp. 950-953 ◽  
Author(s):  
Dawn H. Sephton ◽  
William R. Driedzic
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Whole Blood ◽  
Glycolytic Enzyme ◽  
Adrenergic Stimulation ◽  
Enzyme Binding ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Cell Membrane Binding ◽  
Stimulation Of

Whole blood from rainbow trout (Oncorhynchus mykiss) was incubated in vitro with pharmacological levels of isoproterenol. The adrenergic stimulation of glycolysis in erythrocytes (RBCs) was assessed by monitoring the rate of 14C incorporation from [6-14C]-glucose into the acid-soluble RBC fraction. During a 3-h in vitro incubation, incorporation of label into the acid-soluble RBC fraction of isoproterenol-treated whole blood (0.25 ± 0.04 μmol glucose∙mL−1 RBC∙h−1) was higher than into untreated blood (0.08 ± 0.01 μmol glucose∙mL−1 RBC∙h−1). The percentage of cell membrane binding for phosphofructokinase, aldolase, and glyceraldehyde-3-phosphate dehydrogenase ranged from 17 to 35% and was not altered by adrenergic stimulation. Adrenergic stimulation activates glycolysis in rainbow trout RBCs but not through the modulation of enzyme binding.

Acute inhibition of rat heart protein synthesis in vitro during beta-adrenergic stimulation or hypoxia

1988 ◽  
Vol 255 (4) ◽  
pp. E537-E547 ◽  
Author(s):  
S. J. Fuller ◽  
P. H. Sugden
Keyword(s):  
Protein Synthesis ◽  
Rat Heart ◽  
Energy Status ◽  
Adrenergic Stimulation ◽  
Lactate Output ◽  
Inhibition Of Protein Synthesis ◽  
Cardiac Energy ◽  
Stimulation Of

In the anterogradely perfused rat heart with glucose as fuel, 1 microM isoproterenol (ISO) inhibited the insulin (INS) plus adenosine deaminase (AdoDA) stimulation of ventricular protein synthesis by 72%. ISO (1 microM) alone had no effect on ventricular protein synthesis but inhibited atrial protein synthesis by 20%. The concentration dependence of the ISO inhibition was similar to the stimulation of glucose uptake by ISO. Inhibition could not be overcome by increasing INS concentrations. The effects of ISO were diminished by propranolol and could be partially mimicked by forskolin (FSK) or 8-(4-chlorophenylthio-)adenosine 3',5'-cyclic monophosphate (CPT-cAMP). The stimulation of protein synthesis by noncarbohydrate fuels was antagonized by ISO. Hypoxia (PO2 = 50%) also antagonized the INS stimulation of ventricular protein synthesis but did not affect basal rates. ATP contents were decreased by ISO but not by a PO2 of 50%. Both manipulations increased lactate output. The inhibition of protein synthesis by ISO could possibly be explained by indirect effects of ISO on cardiac "energy status." Furthermore, inhibition may thus represent purely an in vitro phenomenon and may not occur in vivo. However, the possibility that there are more direct effects of ISO on the machinery of protein synthesis has not been excluded. The inhibition of protein synthesis by hypoxia cannot be explained by changes in energy status and may result from intracellular lactoacidosis.

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