scholarly journals Mitogen-stimulated glucose transport in thymocytes. Possible role of Ca++ and antagonism by adenosine 3':5'-monophosphate.

1977 ◽  
Vol 72 (2) ◽  
pp. 456-469 ◽  
Author(s):  
R R Whitesell ◽  
R A Johnson ◽  
H L Tarpley ◽  
D M Regen
Keyword(s):  
Glucose Transport ◽  
Divalent Cations ◽  
Con A ◽  
Cellular Compartment ◽  
Regulatory Processes ◽  
A 23187 ◽  
Camp Levels ◽  
Cellular Ca ◽  
Stimulation Of

The plant lectin, concanavalin A (Con-A), and the ionophore, A-23187 (specific for divalent cations), stimulated glucose transport in rat thymocytes. Con-A stimulation developed more slowly and was somewhat less extensive than that of stimulation developed more slowly and was somewhat less extensive than that of A-23187. Both responses showed saturation dose dependencies. The two responses were poorly additive, suggesting that A-23187 may saturate regulatory processes shared by the two stimulatory mechanisms. Doses of methylisobutylxanthine (MIX) and prostaglandin E2 which raised adenosine 3':5'-monophosphate (cAMP) levels in these cells also antagonized the Con-A stimulation of glucose transport but did not inhibit basal glucose transport or the A-23187 stimulation. Dibutyryl-cAMP and 8-bromo-cAMP also natagonized Con-A stimulation without inhibiting basal glucose transport. MIX antagonized high Con-A doses about as strongly as it did low Con-A doses, suggesting that MIX did not compete in the Con-A binding step or other process saturable by Con-A. [3H-A1Con-A binding was not affected by MIX. The stimulatory effects of Con-A and A-23187 were reduced by reduction of Ca++ in the medium. Both Con-A and A-23187 enhanced 45Ca++ influx and cellular Ca++ content. The A-23187 dose, which was saturating for glucose transport stimulation, enhanced Ca++ influx and cellular Ca++ content more than did the Con-A dose which was saturating for glucose transport stimulation. The dose fo MIX which specifically antagonized Con-A stimulation of glucose transport proved also to reduce Ca++ influx and cellular Ca++ in the presence of Con-A but not in the presence of A-23187. Thus, glucose transport correlates rather well with cellular Ca++. These results are compatible with the view that Ca++ in a cellular compartment can promote glucose transport, the Con-A's enhancement of Ca++ entry contributes to its stimulation of glucose transport, and the MIX antagonized Con-A action at least partly by reducing Ca++ entry. The action of MIX is apparently mediated by cAMP.

The Role of Calcium Ions in the Activation of Blood Platelets

1975 ◽  
Author(s):  
P. Massini
Keyword(s):  
Calcium Ions ◽  
Shape Change ◽  
Divalent Cations ◽  
Blood Platelets ◽  
Clot Retraction ◽  
Release Reaction ◽  
A 23187 ◽  
External Stimuli ◽  
Stimulation Of

The plasma membrane of the resting platelet is only slightly permeable to Ca2+-ions. Stimulation of platelets with thrombin or other activators induces an increased influx of 45Ca. The influx occurs simultaneously with the release of serotonin. The “Ca influx is inhibited when the energy supply of the platelets has been interrupted. Stimulation with thrombin increases the efflux of 46Ca in platelets which have been labelled with 45Ca for 24 hours.Ionophores for divalent cations (X-537 A, A 23187) induce the release reaction, aggregation, clot retraction and rapid shape change. The release reaction does not require external Ca2+-ions whereas clot retraction depends on a Ca2+-eontaining medium.These results strongly suggest that the reactivity of platelets to external stimuli is primarily mediated by an increase of the cytoplasmic concentration of Ca2+-ions.

The Regulatory Role Of Camp In Induction Of Human Platelet Receptor For Fibrinogen

1981 ◽  
Author(s):  
S E Graber ◽  
J Hawiger
Keyword(s):  
Human Platelets ◽  
Membrane Receptor ◽  
Fibrinogen Receptor ◽  
Fibrinogen Binding ◽  
Platelet Receptor ◽  
The Relationship ◽  
Camp Levels ◽  
Dose Dependent ◽  
Stimulation Of

Membrane receptor for fibrinogen plays an essential role in adhesion and aggregation of human platelets by allowing fibrinogen to bridge two or more platelets together. Whereas in normal, unstimulated platelets fibrinogen receptor is not available, it becomes mobilized upon stimulation of platelets with thrombin, ADP, and other stimuli. The mechanism(s) regulating availability of membrane receptor for fibrinogen remains unknown. Following our recent demonstration that prostacyclin (PGI2) prevents mobilization of fibrinogen receptor by thrombin and ADP (Nature 1980, 283,195), we investigated the relationship between cAMP levels and fibrinogen receptor availability. Platelets separated from plasma proteins were briefly exposed to a low thrombin concentration (0.05 U/ml) followed by hirudin to inactivate free thrombin. Binding of 125I-fi- brinogen and cAMP levels were determined in parallel samples. A dose-dependent rise in platelet cAMP levels from 3.3 pM to 10.3 pM/108 platelets in response to PGI2 (3×10-9M - 3×108M) was accompanied by a corresponding inhibition of 125I-fibrinogen binding. The degree of the cAMP increment correlated with binding inhibition (r=0.96). The inhibition of 125I-fibrinogen binding by PGI2 was sustained up to 120 min and was paralleled by a persistent rise in cAMP level. Stimulation of platelet cAMP synthesis “from within” by a ribosylation of the nucleotide regulatory component with subunit A1 of cholera toxin also increased cAMP levels and inhibited fibrinogen receptor mobilization.These results provide evidence that “up and down” regulation of fibrinogen receptor in platelets is linked to changes in cAMP levels induced by different types of adenyl cyclase antagonists and agonists.

scholarly journals Stimulation of glucose transport in Clone 9 cells by insulin and thyroid hormone: role of GLUT-1 activation

1996 ◽  
Vol 1314 (1-2) ◽  
pp. 140-146 ◽  
Author(s):  
Mangala Shetty ◽  
Ashok K Kuruvilla ◽  
Faramarz Ismail-Beigi ◽  
John N Loeb
Keyword(s):  
Thyroid Hormone ◽  
Glucose Transport ◽  
Glut 1 ◽  
Stimulation Of

A forty-year memoir of research on the regulation of glucose transport into muscle

2003 ◽  
Vol 284 (3) ◽  
pp. E453-E467 ◽  
Author(s):  
John O. Holloszy
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Transport ◽  
Historical Review ◽  
Additive Effects ◽  
Glut4 Translocation ◽  
Glut4 Expression ◽  
Exercise Muscle ◽  
Stimulation Of

This historical review describes the research on the regulation of glucose transport in skeletal muscle conducted in my laboratory and in collaboration with a number of colleagues in other laboratories. This research includes studies of stimulation of glucose transport, GLUT4 translocation, and GLUT4 expression by exercise/muscle contractions, the role of Ca2+ in these processes, and the interactions between the effects of exercise and insulin. Among the last are the additive effects of insulin and contractions on glucose transport and GLUT4 translocation and the increases in muscle insulin sensitivity and responsiveness induced by exercise.

Low temperature effects on grapevine photosynthesis: the role of inorganic phosphate

2004 ◽  
Vol 31 (8) ◽  
pp. 789 ◽  
Author(s):  
Luke Hendrickson ◽  
Wah Soon Chow ◽  
Robert T. Furbank
Keyword(s):  
Low Temperature ◽  
Carbon Assimilation ◽  
O2 Evolution ◽  
Vitis Vinifera L ◽  
Regulatory Processes ◽  
Photosynthetic O2 Evolution ◽  
Grapevine Leaves ◽  
Sugar Levels ◽  
Stimulation Of

The photosynthetic response of grapevine leaves (Vitis vinifera L. cv. Riesling) to low temperature was studied to determine the role of end-product limitation and orthophosphate (Pi) recycling to the chloroplast under these conditions. As reported previously, the response of photosynthesis in air to stomatal conductance declined at temperatures below 15°C, suggesting that at low temperatures inhibition of photosynthesis in grapevine has a strong non-stomatal component. Stimulation of carbon assimilation at ambient CO2 by reducing O2 from 21 to 2 kPa, O2 declined to zero below 15°C, a phenomenon often associated with a restriction in photosynthesis due to end-product-synthesis limitation. This stimulation could be restored by feeding Pi. Photosynthesis in leaf disks at both high and low irradiances in non-photorespiratory conditions (1% CO2) was highly sensitive to reductions in temperature. Below 15°C, feeding Pi caused a large stimulation of photosynthetic O2 evolution. Metabolite measurements indicated that despite a decline in Rubisco carbamylation state, ribulose 1,5-bisphosphate (RuBP) levels dropped at low temperature and the ratio of 3-phosphoglycerate (3-PGA) to triose phosphate (TP) remained largely unchanged. These results suggest that grapevine-leaf photosynthesis is severely restricted at low temperature by non-stomatal mechanisms. The return of Pi to the chloroplast plays an important role in this limitation but a coordinated set of regulatory processes maintain a homeostasis of phosphorylated sugar levels.

Stimulation of prolactin release by dopamine withdrawal: role of calcium influx

1994 ◽  
Vol 267 (5) ◽  
pp. E789-E794 ◽  
Author(s):  
K. A. Gregerson ◽  
R. Chuknyiska ◽  
N. Golesorkhi
Keyword(s):  
Channel Blocker ◽  
Inositol Phosphates ◽  
Calcium Influx ◽  
Pituitary Cells ◽  
Induced Changes ◽  
Camp Levels ◽  
Ca2 Channels ◽  
Stimulation Of ◽  
Spiking Activity

Withdrawal of dopamine (DA), a neurotransmitter that inhibits prolactin (PRL) release from the anterior pituitary, stimulates PRL release with transient (30- to 45-min) secretory rates that exceed those observed before application of DA ("PRL rebound"). Using patch-clamp methods on identified rat lactotropes, we have demonstrated that a period of increased Ca(2+)-spiking activity follows recovery from the DA-induced hyperpolarization. The present experiments used dissociated pituitary cells to identify the relative roles of adenosine 3',5'-cyclic monophosphate (cAMP), inositol phosphates, and the enhanced influx of Ca2+ in the rebound secretion of PRL. Rebound secretion of PRL after DA withdrawal was completely blocked by the Ca2+ channel blocker verapamil (20 microM), which also inhibited spontaneous Ca(2+)-spiking activity. DA-induced changes in cAMP levels could be completely dissociated from the PRL rebound. Production of inositol phosphates rose after DA withdrawal but was secondary to the influx of Ca2+. These data demonstrate that influx of extracellular Ca2+ through verapamil-sensitive channels is a critical step in inducing PRL release after DA withdrawal. This finding supports our theory that DA-induced hyperpolarization recruits previously inactivated Ca2+ channels and upon DA washout the enhanced influx of Ca2+ through these voltage-regulated channels supports the rebound release of PRL.

Role of calcium in osmotic and nonosmotic release of vasopressin from rat organ culture

1983 ◽  
Vol 244 (5) ◽  
pp. R703-R708
Author(s):  
S. Ishikawa ◽  
R. W. Schrier
Keyword(s):  
Angiotensin Ii ◽  
Organ Culture ◽  
Arginine Vasopressin ◽  
Ionophore A23187 ◽  
Ang Ii ◽  
Ca Uptake ◽  
High Concentrations ◽  
Cellular Ca ◽  
Stimulation Of

In the present study the role of calcium (Ca) in the stimulation of arginine vasopressin (AVP) release from the cultured rat hypothalamoneurohypophyseal complex (HNC) was examined in response to three different stimuli, 56 mM potassium chloride, an increase in medium osmolality from 290 to 310 mosmol/kg H2O, or 1 X 10(-6) M angiotensin II (ANG II). With all three stimuli AVP release from rat HNC explants was enhanced by increasing Ca concentration in the medium from 0 to 1.8 mM Ca. However, high concentrations of Ca (8 mM) inhibited the response of AVP release to either hyperosmolality or angiotensin II. Chemically dissimilar blockers of cellular Ca uptake, verapamil (5.2 X 10(-6) or 5.2 X 10(-5) M) or nifedipine (5.8 X 10(-6) or 5.8 X 10(-5) M), completely abolished AVP release from rat HNC explants in response to the three different stimuli in 1.8 mM Ca. In a normal concentration of medium Ca (1.8 mM) a Ca ionophore, A23187 (3.8 X 10(-5) M), significantly enhanced the osmotic and nonosmotic (ANG II-stimulated) release of AVP from rat HNC explants compared with controls without Ca ionophore. This effect of Ca ionophore to enhance AVP release was more evident in a lower Ca medium (0.9 mM Ca in the hyperosmolality study and 0.3 mM Ca in the ANG II study). These results therefore indicate that cellular Ca uptake is an important modulator of osmotic and nonosmotic AVP release from the intact rat hypothalamoneurohypophyseal system. The influence of extracellular Ca on the osmotic and nonosmotic release of AVP is also demonstrated.

scholarly journals Characterization of the role of the AMP-activated protein kinase in the stimulation of glucose transport in skeletal muscle cells

2002 ◽  
Vol 363 (1) ◽  
pp. 167 ◽  
Author(s):  
Lee G. D. FRYER ◽  
Fabienne FOUFELLE ◽  
Kay BARNES ◽  
Stephen A. BALDWIN ◽  
Angela WOODS ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Glucose Transport ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Amp Activated Protein Kinase ◽  
Stimulation Of

Forskolin and thyrotrophin stimulation of rat FRTL-5 thyroid cell growth: the role of cyclic AMP

1987 ◽  
Vol 114 (2) ◽  
pp. 199-205 ◽  
Author(s):  
P. A. Ealey ◽  
C. A. Ahene ◽  
J. M. Emmerson ◽  
N. J. Marshall
Keyword(s):  
Cyclic Amp ◽  
Dose Range ◽  
Phosphodiesterase Inhibitor ◽  
Lag Phase ◽  
Thyroid Cell ◽  
Intracellular Camp ◽  
Camp Levels ◽  
Tsh Stimulation ◽  
Stimulation Of

ABSTRACT The adenylate cyclase stimulator forskolin increases intracellular cyclic AMP (cAMP) in rat FRTL-5 cells within minutes and, after a lag phase of 20–24 h, an increase of cells in metaphase is seen. The dose– response relationships were similar in both systems, with significant increases in the number of metaphases observed at ∼0·1 μmol/l and a doubling of cAMP levels at 1 μmol/l, whilst doses of 0·1 mmol/l and above proved cytotoxic. An involvement of intracellular cAMP as a positive intermediate in cell division was further suggested by the finding that a low dose of forskolin (0·1 μmol/l) potentiated TSH stimulation of mitosis. Isobutyl methyl xanthine (IBMX), a phosphodiesterase inhibitor, also acted as a mitogen and potentiated TSH action. Moreover, the simultaneous inclusion of low doses of IBMX and forskolin additionally potentiated TSH stimulation of mitosis. An analogue of cAMP, dibutyryl cAMP, also stimulated mitosis and acted over a restricted dose range, with maximal stimulation at 1 mmol/l. We conclude that cAMP may act as a positive signal for FRTL-5 thyroid cell proliferation. J. Endocr. (1987) 114, 199–205

Role of kinases in insulin stimulation of glucose transport

1989 ◽  
Vol 111 (1) ◽  
pp. 1-23 ◽  
Author(s):  
Amira Klip ◽  
Andre G. Douen
Keyword(s):  
Glucose Transport ◽  
Insulin Stimulation ◽  
Stimulation Of
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