Adaptive changes in the calorigenic effect of catecholamines: Role of changes in the adenyl cyclase system and of changes in the mitochondria

1975 ◽  
Vol 6 (1) ◽  
pp. 15-31 ◽  
Author(s):  
J. Himms-Hagen ◽  
W. Behrens ◽  
M. Muirhead ◽  
A. Hbous
Keyword(s):  
Adenyl Cyclase ◽  
Adaptive Changes ◽  
Adenyl Cyclase System

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.

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.

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.

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