Role of Prostaglandins and Adenosine 3′:5′-Cyclic Monophosphate in the Control by Insulin of Growth-Hormone Synthesis in vitro

1977 ◽  
Vol 5 (1) ◽  
pp. 224-226 ◽  
Author(s):  
ALAN BETTERIDGE ◽  
MICHAEL WALLIS
1973 ◽  
Vol 134 (4) ◽  
pp. 1103-1113 ◽  
Author(s):  
A. Betteridge ◽  
M. Wallis

The effect of insulin on the incorporation of radioactive leucine into growth hormone was investigated by using rat anterior pituitary glands incubated in vitro. A 50% stimulation over control values was observed at insulin concentrations above 2μm (280munits/ml). The effect was specific for growth hormone biosynthesis, over the range 1–5μm-insulin (140–700munits/ml). Lower more physiological concentrations had no significant effect in this system. Above 10μm (1.4 units/ml) total protein synthesis was also increased. The stimulation of growth hormone synthesis could be partially blocked by the addition of actinomycin D, suggesting that RNA synthesis was involved. Insulin was found to stimulate the rate of glucose utilization in a similar way to growth hormone synthesis. 2-Deoxyglucose and phloridzin, which both prevented insulin from stimulating glucose utilization, also prevented the effect of insulin on growth hormone synthesis. If glucose was replaced by fructose in the medium, the effect of insulin on growth hormone synthesis was decreased. We conclude that the rate of utilization of glucose may be an important step in mediating the effect of insulin on growth hormone synthesis.


2009 ◽  
Vol 390 (4) ◽  
pp. 1377-1381 ◽  
Author(s):  
Yolanda Pazos ◽  
Carlos J.P. Álvarez ◽  
Jesús P. Camiña ◽  
Omar Al-Massadi ◽  
Luísa M. Seoane ◽  
...  

1971 ◽  
Vol 124 (4) ◽  
pp. 815-826 ◽  
Author(s):  
R. B. Lockhart Ewart ◽  
K. W. Taylor

1. The release of growth hormone from isolated fragments of rat anterior pituitary tissue incubated in vitro was studied by employing a double-antibody radioimmunoassay. 2. In the absence of added stimuli, two phases of hormone release could be distinguished, an early phase of 2h duration and a subsequent late phase. In the early phase, hormone release was rapid but could be significantly decreased by calcium depletion and by 2,4-dinitrophenol whereas the rate of release in the late phase was uninfluenced by these incubation conditions. These results have been interpreted as indicating the existence of a secretory component in the early phase of release. 3. In subsequent experiments, the effects of various agents on the rate of hormone output during the late phase of incubation were investigated. Hormone release was increased by theophylline and by dibutyryl cyclic AMP (N6-2′-O-dibutyryl-adenosine 3′:5′-cyclic monophosphate), the response to both of these agents being related to the concentration of the stimulant employed. 4. The stimulation of growth hormone output by theophylline was significantly decreased by calcium deprivation and by 2,4-dinitrophenol. The response to dibutyryl cyclic AMP was diminished by 2,4-dinitrophenol, iodoacetate and 2-deoxyglucose but not by malonate or colchicine. 5. Arginine, β-hydroxybutyrate, albumin-bound palmitate and variation in the glucose concentration of the incubation medium over a wide range were without any statistically significant effect on the rate of hormone release from either control pituitary fragments or those subject to secretory stimulation by dibutyryl cyclic AMP. 6. It is suggested that the regulation of growth hormone secretion is mediated by cyclic AMP (adenosine 3′:5′-cyclic monophosphate). The secretion observed in response to cyclic AMP requires the presence of ionized calcium and a source of metabolic energy but is independent of pituitary protein synthesis de novo. The integrity of the glycolytic pathway of glucose metabolism appears to be essential for cyclic AMP-stimulated growth hormone secretion to occur.


1980 ◽  
Vol 239 (4) ◽  
pp. G255-G260
Author(s):  
E. B. Ekblad

Data are presented in support of the role of histamine and adenosine 3',5'-cyclic monophosphate (cAMP) as mediators of acetylcholine-induced acid secretion in frog gastric mucosa. These data also support the notion that acetylcholine-induced alkaline secretion is mediated by guanosine 3',5'-cyclic monophosphate (cGMP). Tissue cAMP and cGMP and rates of acid secretion and histamine release were measured in in vitro preparations of frog gastric mucosa that had been stimulated by acetylcholine. A transient increase in each variable was observed, the sequence of transient maxima being histamine release, cGMP, cAMP, and acid secretion. Atropine, an anticholnergic agent, eliminated all four transient increases, the variables remaining at resting levels. Metiamide, a H2-antagonist, modified the changes observed after acetylcholine stimulation. The acid secretion transience was abolished and the transient increase in tissue cAMP was greatly diminished, whereas the tissue of cGMP transience and histamine release transience remained unchanged. A model is proposed in which acetylcholine initiates two different processes, acid and alkaline secretions.


1988 ◽  
Vol 255 (3) ◽  
pp. F474-F478 ◽  
Author(s):  
W. L. Henrich ◽  
E. A. McAllister ◽  
P. B. Smith ◽  
W. B. Campbell

The role of guanosine 3',5'-cyclic monophosphate (cGMP) as an inhibitory mediator of tissue renin release was examined in two different in vitro preparations. In rat superficial cortical slices, renin release stimulated by isoproterenol (10(-5) M) was ablated by atriopeptin III (ANP, 2.1 x 10(-8) M), nitroprusside (NP, 10(-3) M), and 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP, 10(-3) and 10(-6) M). Arachidonic acid (10(-3) M)-stimulated renin release was also inhibited by ANP and 8-BrcGMP (10(-3) and 10(-6) M). Both ANP and NP increased tissue cGMP concentrations significantly (P less than 0.05), but neither had an effect on adenosine 3',5'-cyclic monophosphate (cAMP) concentrations. When methylene blue (10(-5) M), an inhibitor of guanylate cyclase, was added to slices incubated with isoproterenol and ANP, the inhibition of renin release by ANP was abolished. These results were confirmed in a preparation of isolated cultured rat juxtaglomerular cells. In these cells, isoproterenol induced a significant increase (58%, P less than 0.01) in renin release, which was inhibited by the addition of 8-BrcGMP (10(-6) M). These data demonstrate a direct inhibitory effect of ANP on isoproterenol- and arachidonic acid-induced renin release. The results with NP, 8-BrcGMP, and methylene blue suggest that cGMP is an intracellular mediator of this inhibition.


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