Role of the adenyl cyclase system in stimulation of immunogenesis by bacterial lipopolysaccharide and by endogenous serum pyrogen

1976 ◽  
Vol 81 (5) ◽  
pp. 718-719 ◽  
Author(s):  
O. Sh. Dzheksenbaev ◽  
V. P. Selezneva ◽  
V. T. Loginova
Keyword(s):  
Adenyl Cyclase ◽  
Bacterial Lipopolysaccharide ◽  
Adenyl Cyclase System ◽  
Endogenous Serum Pyrogen ◽  
Stimulation Of Immunogenesis ◽  
Stimulation Of

scholarly journals Lanthanum: inhibition of ACTH-stimulated cyclic AMP and corticosterone synthesis in isolated rat adrenocortical cells.

1976 ◽  
Vol 68 (1) ◽  
pp. 142-153 ◽  
Author(s):  
A Haksar ◽  
D V Maudsley ◽  
F G Péron ◽  
E Bedigian
Keyword(s):  
Cyclic Amp ◽  
Adrenal Cortex ◽  
Binding Sites ◽  
Adenyl Cyclase ◽  
Microscope Examination ◽  
Ca Antagonist ◽  
Corticosterone Response ◽  
Adenyl Cyclase System ◽  
Stimulation Of

Lanthanum (La+++) is a well-known Ca++ antagonist in a number of biological systems. It was used in the present study to examine the role of Ca++ in the regulation of adenyl cyclase of the adrenal cortex by ACTH. In micromolar concentrations, .La+++ inhibited both cyclic AMP and corticosterone response of isolated adrenal cortex cells to ACTH. However, a number of intracellular processes were not affected by La+++. These include the stimulation of steroidogenesis by dibutyryl cyclic AMP, conversion of several steroid precursors into corticosterone, and stimulation of the latter by glucose. Thus, inhibition of steroidogenesis by La+++ appears to be solely due to an inhibition of ACTH-stimulated cyclic AMP formation. Electron microscope examination showed that La+++ was localized on plasma membrane of the cells and did not appear to penetrate beyond this region. Since La+++ is believed to replace Ca++ at superficial binding sites on the cell membrane, it is proposed that Ca++ at these sites plays an important role in the regulation of adenyl cyclase by ACTH. Similarities in the role of Ca++ in "excitation-contraction" coupling and in the ACTH-adenyl cyclase system raise the possibility that a contractile protein may be involved in the regulation of adenyl cyclase by those hormones which are known to require Ca++ in the process.

Transepithelial Potential Changes During Stimulation of Isolated Salivary Glands with 5-Hydroxytryptamine and Cyclic Amp

1972 ◽  
Vol 56 (1) ◽  
pp. 139-153
Author(s):  
MICHAEL J. BERRIDGE ◽  
WILLIAM T. PRINCE
Keyword(s):  
Cyclic Amp ◽  
Salivary Glands ◽  
Electrical Response ◽  
Cation Transport ◽  
Anion Transport ◽  
Adenyl Cyclase ◽  
Positive Potential ◽  
Dose Dependent ◽  
Stimulation Of

1. The role of cyclic AMP in mediating the action of 5-HT on salivary glands has been studied by measuring transepithelial potentials. 2. The lumen of unstimulated glands is 4 mV positive but becomes 12 mV negative after treatment with 5-HT (10-8M). Both the potential and the secretory responses to 5-HT are dose-dependent over the same concentration range. 3. The electrical response of salivary glands to cyclic AMP is qualitatively different to that of 5-HT; instead of going negative the potential goes more positive. 4. An increase in positive potential is also observed after treatment with theophylline (10-2M), or when glands are stimulated with 5-HT in a chloride-free saline. 5. These results are consistent with the idea that 5-HT has two actions. One is to stimulate the enzyme adenyl cyclase to synthesize cyclic AMP, which, in turn, stimulates cation transport. The other is to increase anion transport by a mechanism which is independent of cyclic AMP.

BABIES, HORMONES AND KIDNEYS—A NEW LOOK AT DEVELOPMENT

PEDIATRICS ◽  
1972 ◽  
Vol 50 (1) ◽  
pp. 3-4
Author(s):  
Wallace W. McCrory
Keyword(s):  
Cyclic Amp ◽  
Rat Kidney ◽  
Adenyl Cyclase ◽  
Endocrine Gland ◽  
Hormone Action ◽  
Abundant Evidence ◽  
Cell Target ◽  
Urinary Cyclic Amp ◽  
Adenyl Cyclase System

The role of cyclic AMP (adenosine 3’,5’-monophosphate) in hormone action is now quite firmly established. Abundant evidence now demonstrates that after release from an endocrine gland a hormone (first messenger) is transported to its effector cell (target) where it interacts with the adenyl cyclase system to release cyclic AMP (second messenger) which acts intracellularly to carry out the work of the hormone. In 1967, Chase and Aurbach demonstrated that urinary cyclic AMP, now known to be derived from both plasma and kidney, increased when parathormone (PTH) was administered to the rat and man. These workers also demonstrated a PTH-sensitive adenyl cyclase in the proximal tubules of the rat kidney and in fetal bone.

A POSSIBLE ROLE FOR THE ADENYL CYCLASE SYSTEM IN CALCITONIN RELEASE

1970 ◽  
Vol 48 (1) ◽  
pp. 1-15 ◽  
Author(s):  
A. D. CARE ◽  
R. F. L. BATES ◽  
H. J. GITELMAN
Keyword(s):  
Cyclic Guanosine Monophosphate ◽  
Adenyl Cyclase ◽  
Guanosine Monophosphate ◽  
Adrenergic Blockade ◽  
Significant Stimulation ◽  
Thyroid Glands ◽  
Plasma Calcium Concentration ◽  
Adenyl Cyclase System

SUMMARY A possible role of the adenyl cyclase system in calcitonin (CT) release has been investigated by measurement of the rate of CT secretion in isolated porcine thyroid glands perfused in situ. Dibutyryl cyclic AMP increased the rate of secretion of CT and this effect was enhanced by theophylline. Concentrations of glucagon as low as 1·4 nm (5 ng/ml) induced a significant increase in the rate of CT secretion when precautions were taken to prevent enzymic degradation of glucagon. This stimulatory effect of glucagon on CT secretion was also increased by theophylline. Significant stimulation of CT release was demonstrated with adrenaline in the presence of α-adrenergic blockade with phentolamine and could be inhibited by β-adrenergic blockade with propranolol. In contrast, thyrotrophin, tri-iodothyronine, serotonin, parathyroid hormone and cyclic guanosine monophosphate had no significant acute effects on CT secretion. It is suggested that the C-cells of the thyroid gland contain an adenyl cyclase system similar to that described in other tissues and that physiological concentrations of glucagon and catecholamines may influence the response of the C-cell to plasma calcium concentration.

A Study of the Neurohumoral Control of Glycolysis in the Mouse Brain in vivo: Role of Noradrenaline and Dopamine

1975 ◽  
Vol 30 (5-6) ◽  
pp. 385-391 ◽  
Author(s):  
B. E. Leonard
Keyword(s):  
Mouse Brain ◽  
Sodium Fluoride ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Adenyl Cyclase ◽  
Membrane Bound ◽  
Adenyl Cyclase System ◽  
Neurohumoral Control

Abstract Noradrenaline, Dopamine, Glycolysis, Adenyl Cyclase Intraventricularly injected noradrenaline, dopamine and isoprenaline increased glycolysis as shown by the decrease in the concentration of “free” glycogen and increase in the concentration of lactate. The effects of noradrenaline and isoprenaline were reduced in mice which had been pretreated with α-methyl-p-tyrosine. ʟᴅ-Propranolol blocked the increase in glycolysis caused by noradrenaline, isoprenaline, sodium fluoride and analogues of 3,5-cyclic adenosine monophosphate. It is suggested that the results of this investigation can be explained by the various drugs and neurohormones acting on the adenyl cyclase system in vivo, either by blocking the action of the neurohormone on the membrane bound enzyme or monophosphate on glycolysis.

Changes in the Adenyl Cyclase System of Skeletal Muscle of Cold-Acclimated Rats

1974 ◽  
Vol 52 (3) ◽  
pp. 176-180 ◽  
Author(s):  
Michelle Muirhead ◽  
Jean Himms-Hagen
Keyword(s):  
Skeletal Muscle ◽  
Plasma Membrane ◽  
Cold Acclimation ◽  
Metabolic Response ◽  
Adenyl Cyclase ◽  
Nonshivering Thermogenesis ◽  
Receptor System ◽  
Adenyl Cyclase System ◽  
Shivering Thermogenesis ◽  
Stimulation Of

No change could be detected in the adenyl cylase system (basal activity, noradrenaline-stimulated activity, adrenaline-stimulated activity, fluoride-stimulated activity) of skeletal muscle of cold-acclimated rats. It is concluded that the enhancement of metabolic response to noradrenaline during cold-acclimation, which occurs principally in skeletal muscle, can not be attributed to an alteration in this component of the receptor system for noradrenaline.An increase in the activity of the catecholamine-stimulated and fluoride-stimulated adenyl cyclase of skeletal muscle occurs during the 1st week of exposure to cold and has disappeared by the time the rats are fully acclimated. This increase coincides with the period of shivering thermogenesis rather than with the development of nonshivering thermogenesis; it may be related to the intense and repeated stimulation of plasma membrane associated with shivering.

scholarly journals The Role of Cyclic Nucleotides and Prostaglandins in the Mechanisms of Aggregation of Thrombocytes

1977 ◽  
Author(s):  
S. V. Andreev ◽  
A. A. Kubatiev ◽  
Ya. D. Mamedov
Keyword(s):  
Comparative Study ◽  
Cyclic Nucleotides ◽  
Initial Level ◽  
Proteolytic Enzymes ◽  
Adenyl Cyclase ◽  
The Other ◽  
Initial Link ◽  
Stimulation Of

In a comparative study into the mechanisms of aggregation of thrombocytes under the influence of various agents, two types of reactions were established, one realized through the system of cyclic 3′5-AMP and the other, through the system of cyclic 3′5-GMP. The former type of reaction was observed when ADP and thrombin were used as aggregation inductors; the latter was induced by serotonin. The initial link in the development of aggregation of thrombocytes induced by ATP and thrombin was an increase in the level of prostaglandin EI (by 32%), under the effect of which the activity of adenyl cyclase rose more than by 41%, and the amount of 3’5-cAMP increased by almost 180% as compared with the initial level. Unlike ADP and thrombin, stimulation of thrombocytes with serotonin brought about, as a rule, an increase in the level of prostaglandins F2 (by 60%) , which subsequently led to activation of guanyl cyclase and marked augmentation in the content of 3′5-cGMP (by 300%). The application of proteolytic enzymes with thrombolytically oriented properties caused inhibition of biosynthesis of prostaglandins and cyclic nucleotides with a clearcut disaggregating effect.

Dependence of Platelet Adenyl Cyclase System on Oxidative Phosphorylation

1975 ◽  
Vol 34 (01) ◽  
pp. 042-049 ◽  
Author(s):  
Shuichi Hashimoto ◽  
Sachiko Shibata ◽  
Bokro Kobayashi
Keyword(s):  
Cyclic Amp ◽  
Oxidative Phosphorylation ◽  
Sodium Succinate ◽  
Potassium Cyanide ◽  
Adenyl Cyclase ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Adenyl Cyclase Activity ◽  
Intact Rabbit ◽  
Adenyl Cyclase System ◽  
Cyclic Amp Synthesis

SummaryThe radioactive adenosine 3′,5′-monophosphate (cyclic AMP) level derived from 8-14C adenine in intact rabbit platelets decreased in the presence of mitochondrial inhibitor (potassium cyanide) or uncoupler (sodium azide), and markedly increased by the addition of NaF, monoiodoacetic acid (MIA), or 2-deoxy-D-glucose. The stimulative effect of the glycolytic inhibitors was distinctly enhanced by the simultaneous addition of sodium succinate. MIA did neither directly stimulate the adenyl cyclase activity nor inhibit the phosphodiesterase activity. These results suggest that cyclic AMP synthesis in platelets is closely linked to mitochondrial oxidative phosphorylation.

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

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